Movatterモバイル変換


[0]ホーム

URL:


CN119082017A - Application of miR-378a-5p in promoting the differentiation of initialized CD4+T cells into Th1 - Google Patents

Application of miR-378a-5p in promoting the differentiation of initialized CD4+T cells into Th1
Download PDF

Info

Publication number
CN119082017A
CN119082017ACN202410868909.2ACN202410868909ACN119082017ACN 119082017 ACN119082017 ACN 119082017ACN 202410868909 ACN202410868909 ACN 202410868909ACN 119082017 ACN119082017 ACN 119082017A
Authority
CN
China
Prior art keywords
mir
braf
cells
differentiation
expression
Prior art date
Legal status (The legal status is an assumption and is not a legal conclusion. Google has not performed a legal analysis and makes no representation as to the accuracy of the status listed.)
Pending
Application number
CN202410868909.2A
Other languages
Chinese (zh)
Inventor
朱明星
赵巍
张婷婷
钱炳硕
穆虎
王川
Current Assignee (The listed assignees may be inaccurate. Google has not performed a legal analysis and makes no representation or warranty as to the accuracy of the list.)
Ningxia Medical University
Original Assignee
Ningxia Medical University
Priority date (The priority date is an assumption and is not a legal conclusion. Google has not performed a legal analysis and makes no representation as to the accuracy of the date listed.)
Filing date
Publication date
Application filed by Ningxia Medical UniversityfiledCriticalNingxia Medical University
Priority to CN202410868909.2ApriorityCriticalpatent/CN119082017A/en
Publication of CN119082017ApublicationCriticalpatent/CN119082017A/en
Pendinglegal-statusCriticalCurrent

Links

Classifications

Landscapes

Abstract

Translated fromChinese

本发明关于细胞工程和基因工程技术领域,尤其涉及miR‑378a‑5p在促进初始化CD4+T细胞向Th1方向分化中的应用。本发明通过研究发现了miR‑378a‑5p能通过调节其靶基因BRAF进而影响初始化CD4+T细胞的分化,并验证了miR‑378a‑5p引起的促进初始化CD4+T细胞向Th1方向分化能够被BRAF恢复。因此,miR‑378a‑5p模拟物可用于促进初始化CD4+T细胞向Th1方向分化,从而可以作为活性成分,用于制备于棘球蚴病预防和治疗药物。

The present invention relates to the field of cell engineering and genetic engineering technology, and in particular to the application of miR‑378a‑5p in promoting the differentiation of initialized CD4+ T cells in the direction of Th1. The present invention has found through research that miR‑378a‑5p can affect the differentiation of initialized CD4+ T cells by regulating its target gene BRAF, and verified that the promotion of the differentiation of initialized CD4+ T cells in the direction of Th1 caused by miR‑378a‑5p can be restored by BRAF. Therefore, miR‑378a‑5p mimics can be used to promote the differentiation of initialized CD4+ T cells in the direction of Th1, and thus can be used as an active ingredient for the preparation of drugs for the prevention and treatment of echinococcosis.

Description

Application of miR-378a-5p in promotion of initialization of differentiation of CD4 + T cells to Th1 direction
Technical Field
The invention relates to the technical field of biology, in particular to application of miR-378a-5p in promotion of differentiation of initialized CD4+ T cells to Th1 direction.
Background
Echinococcosis, also known as echinococcosis, is a parasitic disease of both humans and animals caused by the parasitic larvae of echinococcosis in hosts, and occurs mainly in countries and regions where animal husbandry is developed. When the host is infected with echinococci, the host will produce very complex immune responses, including humoral, cellular and complement-mediated immune responses. Among them, CD4+ T cells play an important role in the correlation of echinococcosis with host. In early prevention studies, studies of genetically engineered vaccines have been of great interest.
The discovery of non-coding RNAs (ncrnas) has a significant impact on the study of gene expression regulation. Although they lack protein-encoding capacity, they can regulate gene expression and protein function, and are involved in various biological mechanisms including growth, migration, autophagy, apoptosis, differentiation, and the like. The microRNA is a single-stranded non-coding small RNA molecule with the length of about 22 nucleotides widely expressed in cells, and the target mRNA is degraded or the translation of the target mRNA is inhibited mainly through specific interaction with a 3' -untranslated region of a target gene, so that the formation of the target protein is blocked, and the regulation and control effects of the target protein are exerted. In recent years, increasing research has revealed that mirnas are involved in the development of a variety of diseases, including different types of cancer, heart diseases (such as hypertrophy and ischemia), and diseases associated with mental disorders (such as schizophrenia or major depression). It was found that parasitic infections can also cause changes in host mirnas, thereby modulating expression of a range of host genes, thereby evading host immune defenses.
Disclosure of Invention
Aiming at the technical problems, the invention provides application of miR-378a-5p in promoting the differentiation of an initialized CD4+ T cell to a Th1 direction. According to the invention, research shows that miR-378a-5p can influence the differentiation of the initialized CD4+ T cells by regulating the target gene BRAF, and provides a new clue and theoretical basis for preventing and treating echinococcosis.
In order to achieve the aim of the invention, the invention adopts the following technical scheme:
The first aspect of the invention provides an application of miR-378a-5p in promoting differentiation of initialized CD4+ T cells to Th1 direction.
The invention discovers that the anti-bag worm immune protection force of the echinococcus granulosus recombinant protein P29 (rEg.P29) on mice and sheep is 96.6 percent and 94.5 percent respectively. The rEg.P29 can stimulate the organism to generate humoral immunity and cellular immunity at the same time, the rEg.P29 immunity can induce high-level anti-rEg.P29 specific antibodies, the antibody response reaches a peak at the 2 nd week after the booster immunity and is maintained for more than 16 weeks, and meanwhile, the rEg.P29 can generate a large amount of cytokines such as IFN-gamma and the like to clear pathogens by promoting the differentiation of the initial CD4+ T cells to the Th1 direction. According to the invention, rEg.P29 is taken as an entry point, a artemia infection model and a rEg.P29 immune model of a mouse are constructed, and a second generation sequencing technology is adopted to screen microRNA molecules which are differentially expressed in immune cells of the mouse before and after rEg.P29 immunization and before and after artemia infection. Sequencing results show that compared with the cabbage caterpillar positive infection group, the rEg.P29 immune group with higher protective power has obviously increased mmu-miR-378a-5p expression level. The invention predicts the target gene possibly regulated by miR-378a-5p by using a target gene prediction website, and the target gene is proved to be BRAF by using a dual-luciferase reporter gene. Experiments of qRT-PCR, western blot and flow cytometry prove that miR-378a-5p influences differentiation of initialized CD4+ T cells by regulating BRAF, and further the fact that miR-378a-5p can promote differentiation of initialized CD4+ T cells of a mouse spleen to a Th1 direction and inhibit differentiation of initialized CD4+ T cells to a Th2 direction is further determined.
In order to verify the influence of miR-378a-5p target gene BRAF on the differentiation of initialized CD4+ T cells, the invention also synthesizes an interference small segment siRNA-BRAF-1341 of the target gene BRAF, after the interference small segment is transfected in the initialized CD4+ T cells, the detection results of qRT-PCR, western blot and flow cytometry show that the expression of Th1 type cytokine IFN-gamma is obviously increased, the expression of Th2 type cytokine IL-4 is obviously decreased, and the opposite result is obtained after the transfected BRAF over-expresses lentivirus, which shows that the BRAF inhibits the differentiation of mouse spleen initial CD4+ T cells to the Th1 direction and promotes the differentiation to the Th2 direction.
In order to verify the functional recovery of miR-378a-5p target gene BRAF, the expression of Th1 type cytokines IFN-gamma and Th2 type cytokines IL-4 is detected by qRT-PCR and flow cytometry after the co-transfection of miR-378a-5p and BRAF in mouse spleen initialized CD4+ T cells. As a result, it was found that promotion of differentiation of CD4+ T cells in the Th1 direction, which is initiated by miR-378a-5p, can be restored by BRAF.
Since the experiment was designed to spleen cells, human experiments could not be performed, so the experiment was verified in mouse spleen cells. The mature body sequence of miR-378a-5p is consistent in mice and human bodies, so that the invention provides a new thought and direction for clinically discussing the change of immune mechanism in a patient infected by the Baotou, and provides a new clue and theoretical basis for diagnosis and prevention of echinococcosis.
With reference to the first aspect, the nucleotide sequence of miR-378a-5p is CUCCUGACUCCAGGUCCUGUGU (shown as SEQ ID No: 1).
The second aspect of the invention provides application of miR-378a-5p mimics in preparation of echinococcosis preventing or treating medicines. Because the miR-378a-5p mimic can improve the expression quantity of miR-378a-5p in cells, and miR-378a-5p can promote the initialization of differentiation of CD4+ T cells to the Th1 direction and activate cellular immune response, the miR-378a-5p mimic plays roles in controlling early formation, growth, transfer and anti-infection of bag worm, and can be used for preparing echinococcosis prevention or treatment medicines.
With reference to the second aspect, the miR-378a-5p mimic is double-stranded:
The sense strand sequence is CUCCUGACUCCAGGUCCUGUGU (shown as SEQ ID No. 2);
The antisense strand sequence is ACAGGACCUGGAGUCAGGAGUU (shown as SEQ ID No. 3).
The third aspect of the invention provides a medicine for preventing echinococcosis, the active ingredient of which comprises miR-378a-5p mimics.
With reference to the third aspect, the miR-378a-5p mimic is double-stranded:
The sense strand sequence is CUCCUGACUCCAGGUCCUGUGU;
The antisense strand sequence is ACAGGACCUGGAGUCAGGAGUU.
With reference to the third aspect, the dosage form of the medicament is an injection.
The third aspect of the invention provides a medicament for treating echinococcosis, the active ingredient of which comprises miR-378a-5p mimics.
With reference to the fourth aspect, the miR-378a-5p mimic is double-stranded:
The sense strand sequence is CUCCUGACUCCAGGUCCUGUGU;
The antisense strand sequence is ACAGGACCUGGAGUCAGGAGUU.
In combination with the fourth aspect, the medicament is in the form of an injection.
The invention has the beneficial effects that the initialization of the differentiation of CD4+ T cells has great effect on the host to resist external pathogens, and has important significance on the prevention and treatment of echinococcosis. The invention firstly confirms the effect of miR-378a-5p and BRAF in the process of initiating CD4+ T cell differentiation in the spleen of a mouse and the targeting relation between miR-378a-5p and BRAF, and confirms that the target gene BRAF can restore cell differentiation caused by miR-378a-5p through rescue, thereby proving the effect of miR-378a-5p in the process of initiating CD4+ T cell differentiation in the spleen of the mouse. The invention provides a new clue and theoretical basis for preventing and treating echinococcosis.
Drawings
FIG. 1 is a graph showing the effect of miR-378a-5p mimics and miR-378a-5p inhibitor on miR-378a-5p expression levels, measured by qRT-PCR technology in example 1 of the invention;
FIG. 2 is the differentiation of the CD4+ T cells initiated by the spleen of the mice after transfection of miR-378a-5pmimics and miR-378a-5p inhibitor, which were measured by qRT-PCR technology in example 1 of the invention;
FIG. 3 shows the interference effects of siRNA-BRAF-972, siRNA-BRAF-1341 and siRNA-BRAF-1845/siRNA-NC and OE-BRAF of different interference fragments measured by qRT-PCR technique in example 1 of the present invention;
FIG. 4 shows the differentiation of mouse spleen-initiated CD4+ T cells after transfection of OE-BRAF and siRNA-BRAF-1341 by qRT-PCR technique in example 1 of the present invention;
FIG. 5 is the expression of the Th1 type cytokines IFN-gamma and Th2 type cytokine IL-4 after co-transfection of miR-378a-5p and BRAF in initialized CD4+ T cells, as measured by qRT-PCR technique in example 1 of the invention;
FIG. 6 shows the differentiation of the mouse spleen-initiated CD4+ T cells after transfection of miR-378a-5p mimics and miR-378a-5p inhibitor, which were measured by Western blot in example 1 of the invention;
FIG. 7 shows the differentiation of mouse spleen-initiated CD4+ T cells after transfection of OE-BRAF and siRNA-BRAF-1341 by Western blot in example 1 of the present invention;
FIG. 8 is a graph showing the initiation of differentiation of CD4+ T cells from the spleen of mice after transfection of miR-378a-5p mimics and miR-378a-5p inhibitor, as measured by flow cytometry in example 1 of the invention;
FIG. 9 is the differentiation of mouse spleen-initiated CD4+ T cells after transfection of OE-BRAF and siRNA-BRAF-1341 as measured by flow cytometry in example 1 of the present invention;
FIG. 10 is the expression of the Th1 and Th2 cytokines IFN-gamma and IL-4 following co-transfection of miR-378a-5p and BRAF in initialized CD4+ T cells as measured by flow cytometry in example 1 of the present invention;
FIG. 11 is a graph showing the results of dual fluorescein reporting in example 2 of the present invention;
FIG. 12 shows the results of an animal experiment in example 3 of the present invention.
Detailed Description
The present invention will be described in further detail with reference to specific embodiments in order to make the objects, technical solutions and advantages of the present invention more apparent. It should be understood that the specific embodiments described herein are for purposes of illustration only and are not intended to limit the scope of the invention. All other embodiments, which can be made by those skilled in the art based on the embodiments of the present invention without making any inventive effort, fall within the scope of the present invention.
In the invention, miR-378a-5p mimics (a simulator) represents a simulator of miR-378a-5p, is synthesized by simulating miR-378a-5p in a living body by using a chemical synthesis method, and can enhance the expression quantity of miR-378a-5p. NC (negative control) of miR-378a-5p mimics represents a negative control of miR-378a-5p mimics, i.e., a sequence similar in structure to miR-378a-5p mimics but not meaningless, without over-expression of miR-378a-5p. The transfection of miR-378a-5p mimics with its corresponding NC was performed in order to exclude the effect of transfection of such sequences on the experimental results.
MiR-378a-5p mimics used in the invention is double-stranded:
The sense strand sequence is CUCCUGACUCCAGGUCCUGUGU;
The antisense strand sequence is ACAGGACCUGGAGUCAGGAGUU.
In the invention, miR-378a-5p inhibitor represents an inhibitor of miR-378a-5p, and is a chemically modified inhibitor specifically aiming at miR-378a-5p in cells. NC of miR-378a-5pinhibitor represents a negative control of miR-378a-5p inhibitor, namely a sequence similar to miR-378a-5pinhibitor in structure but nonsensical, and does not influence expression of miR-378a-5 p.
The miR-378a-5p inhibitor used in the invention is single-chain ACACAGGACCUGGAGUCAGGAG.
In the present invention, the NC of miR-378a-5p is an artificially designed double-stranded miRNA molecule, and does not target any known human, mouse and rat genes.
In the present invention, siRNA-NC is a common negative control that has no homology to the sequence of the target gene and has no homology to other genes in the target cell.
The above mimics, inhibitors or NC's may be designed and obtained by those skilled in the art without specific explanation based on conventional knowledge.
The invention is further illustrated by the following examples.
Example 1
In the embodiment, the effect of miR-378a-5p on initiating CD4+ T cell differentiation is verified by using mouse spleen initiating CD4+ T cells, and the targeting relationship between miR-378a-5p and a target gene BRAF is verified.
1. Isolation and culture of mouse spleen-initiated CD4+ T cells:
(1) Grinding spleen, namely dissecting and killing a mouse, taking the spleen aseptically, placing the mouse in a 70 mu m filter membrane, adding sample diluent, lightly grinding the mouse, finally preparing 5ml of cell suspension, and blowing and uniformly mixing the mouse and the sample diluent;
(2) Separating, namely adding 5ml of mouse spleen lymphocyte separating liquid into a 15ml centrifuge tube, tilting the centrifuge tube, slowly adding the cell suspension of the last step into the centrifuge tube twice, centrifuging for 20min at 450xg and 22 ℃;
(3) Cleaning, namely separating the solution into 4 layers after centrifugation, discarding the upper liquid layer, carefully sucking the white membrane layer into another clean centrifuge tube, adding 10ml of cleaning solution, 350xg, and centrifuging at 22 ℃ for 10min, and cleaning twice;
(4) Counting, namely finally, resuspending the count by using a complete culture medium;
(5) After resuspension counting, 40. Mu.L of magnetic bead sorting buffer, 10. Mu.L of magnetic bead sorting buffer was added per 1X 107 cellsCD4+ T Cell Biotin-Antibody Cocktail, incubated at 4℃for 5min in the absence of light;
(6) 20. Mu.L of magnetic bead sorting buffer, 20. Mu.L of Anti-biotin MicroBeads, 10. Mu.L of CD44 microblades were added to each 1X 107 cell, and incubated at 4℃for 10min in the absence of light;
(7) Fixing a sorting column to prepare sorting, operating the process on ice, diluting the incubated cell suspension, firstly wetting the sorting column, then adding a certain amount of magnetic bead sorting buffer, adding the cell suspension for multiple times, and collecting the cell suspension by using a 15ml centrifuge tube;
(8) After sorting, 350Xg,4 ℃, centrifuging for 10min, and then re-suspending with 1640 complete medium for later use.
2. Transfection of miR-378a-5p mimics, inhibitor:
(1) Firstly, dissolving miR-378a-5p mimics, miR-378a-5p inhibitor and negative control according to the specification to form a storage solution with the concentration of 20 mu M;
(2) Anti-CD3 coated in 24-well plates the previous day was then discarded, and initial CD4+ T cells from magnetic bead sorting were plated in well plates (400. Mu.L/well);
(3) The transfection mimic concentration was calculated and the transfection system was formulated as follows in tables 1 and 2:
table 1 transfection System of miR-378a-5p mimics
TABLE 2 transfection of miR-378a-5p inhibitor
(4) After preparing a transfection system, lightly flicking and uniformly mixing fingers, standing at room temperature for 8min, dripping the mixture into a corresponding pore plate according to groups, and placing the mixture into a 37 ℃ and 5% CO2 incubator for culture;
(5) At the time of culturing for 6 hours, cytokines that differentiated the primary CD4+ T lymphocytes in Th1 and Th2 directions were added, respectively, as shown in tables 3 and 4:
TABLE 3Th1 polarization factor
TABLE 4Th2 polarization factor
(6) Culturing is continued for 48 hours, and the cells are harvested for subsequent experiments.
3. Transfection of siRNA-BRAF, OE-BRAF:
The target gene of miR-378a-5p is predicted through a bioinformatics website, and the target gene is proved to be BRAF by the double-luciferase reporter gene. The target genes of miR-378a-5p are predicted by TARGETSCAN, MIRWALK, MIRDB pieces of bioinformatics software, and through double-luciferase report analysis, the BRAF wild type 3' UTR region is controlled by miR-378a-5p, while the mutation is not controlled by miR-378a-5 p.
The interference fragments of the target gene BRAF are respectively siRNA-BRAF-972, siRNA-BRAF-1341 and siRNA-BRAF-1845/siRNA-NC, and the interference efficiency is detected by qRT-PCR. And (3) transfecting the siRNA into a mouse spleen initialized CD4+ T cell, and finally screening out the siRNA-BRAF-1341 fragment with the best interference effect by utilizing a qRT-PCR technology to carry out subsequent experiments. The sequence of the synthesized interference fragment is as follows, siRNA-BRAF-972:sense:5'-CCAACUUGAUUUGCUGUUUTT-3';
Anti-sense:5′-AAACAGCAAAUCAAGUUGGTT-3′;
siRNA-BRAF-1341:Sense:5′-CCAACUGAUGCGCUGUCUUTT-3′;
Anti-sense:5′-AAGACAGCGCAUCAGUUGGTT-3′;
siRNA-BRAF-1845:Sense:5′-GCCACAACUGGCAAUUGUUTT-3′;
Anti-sense:5′-AACAAUUGCCAGUUGUGGCTT-3′。
the above-mentioned interference fragment and control fragment siRNA-NC were synthesized by Shanghai Ji Ma pharmaceutical technologies Co.
Packaging target gene BRAF over-expressed slow virus. Firstly, downloading CDS sequences of BRAF genes at NCBI, delivering Feng Hui to biologically construct BRAF over-expression plasmids, inserting the BRAF over-expression plasmids into pLVX-EGFP-IRES-PURO, taking empty vector as a reference, carrying out plasmid amplification and plasmid extraction, packaging recombinant plasmid lentivirus to obtain the BRAF over-expression lentivirus, and verifying transfection efficiency through qRT-PCR.
SiRNA-BRAF-1341 and OE-BRAF are transfected into mouse spleen initiating CD4+ T cells, and the influence of target gene BRAF on initiating CD4+ T cell differentiation is studied. The siRNA-BRAF transfection system is shown in Table 5.
Table 5siRNA-BRAF transfection system:
Transfection of OE-BRAF 1.5 mu L Lipo 3000 is added per 100 mu L virus, mixed by flick and then kept stand for 10min, then added into cells, cultured for 6h, added with corresponding polarization factors, and further cultured for 48h for subsequent experiments.
4. Cell total RNA extraction and qRT-PCR embodiment:
In the invention, qRT-PCR detection of target genes and miRNA are respectively adoptedBioscience Co LtdOne STEP RT QPCR KIT (Sybr Green) and Ji Ma company miRNA qRT-PCR TBKit。
The total RNA extraction step is described in TRIZOL operating instructions of Thermofisher, and the specific extraction steps are as follows:
(1) Adding 1mL TRIZOL per 1×107 cells, blowing with a pipette until the liquid is clear and no cell mass exists, mixing for about 10 times, and standing at room temperature for 10min;
(2) Adding 200 μl (1/5 volume of the total amount) of chloroform in dark place, vigorously mixing for 15s, and standing at room temperature for 5min;
(3) Centrifugation at 12000Xg,4℃for 15min, carefully aspirate the upper aqueous layer (approximately 400-500. Mu.L, which is contraindicated for aspiration of the middle layer) into a fresh 1.5mL EP tube;
(4) Adding isopropyl alcohol with equal volume, blowing and mixing uniformly, and standing at room temperature for 10min;
(5) Centrifuging at 4deg.C, 12000Xg, and 10min, discarding supernatant (RNA forms white gel-like particles at bottom);
(6) 1mL of precooled 75% alcohol (used as prepared) is added;
(7) Centrifuging at 4 ℃ for 5min at 7500xg, discarding the supernatant (leaving a point at the bottom, sucking the supernatant out by a 10 mu L pipette), and drying by a super clean bench for 5min;
(8) Adding 20-30 mu L of enzyme-free water, taking 1 mu L of RNA to detect purity and content, and using the rest for reverse transcription.
QRT-PCR was performed according to the real-time fluorescent quantitative PCR reagent specifications, the reaction system is shown in Table 6, and the reaction conditions are shown in Table 7.
TABLE 6qRT-PCR reaction System
Table 7qRT-PCR reaction conditions:
The experimental result is used for detecting the content of the sample gene or miRNA by a Ct value comparison method, and the specific calculation formula is as follows:
gene relative expression level=2- { < (test group objective gene Ct value) - (test group internal gene Ct value) > (control group objective gene Ct value) - (control group internal gene Ct value) >
Wherein, the reference gene is used as reference for GAPDH for gene detection and U6 for miRNA detection.
The results are shown in FIG. 1-FIG. 5:
As can be seen from panel A in FIG. 1, the expression of miR-378a-5p was elevated 48h after transfection of miR-378a-5p mimics at different concentration gradients into mouse spleen naive CD4+ T cells, but the expression of miR-378a-5p was no longer increased with increasing concentration when the transfection concentration reached 60 nM.
As can be seen from the graph B in FIG. 1, the miR-378a-5p inhibitor with different concentration gradients is reduced in the expression of miR-378a-5p after being transfected into the initial CD4+ T cells of the spleen of the mouse for 48 hours, wherein the reduction effect is obvious at the concentration of 100nM, and the reduction effect is not obvious at the concentration of 150nM, and the method has no statistical significance.
FIG. 2 shows the differentiation of mice spleen-initiated CD4+ T cells after transfection of 60nM miR-378a-5p mimics or 100nM miR-378a-5pinhibitor to reflect the effect of miR-378a-5p on initiating CD4+ T cell differentiation. As can be seen from FIG. 2, transfection of 60nM miR-378a-5p mimics promoted expression of the Th 1-type cell-representing factor IFN-gamma and transcription factor T-bet (panels A and B) and inhibited expression of the Th 2-type cell-representing factor IL-4 and transcription factor GATA-3 (panels E and F), and transfection of miR-126a-5p inhibitor inhibited expression of the Th 1-type cell-representing factor IFN-gamma and transcription factor T-bet (panels C and D) and promoted expression of the Th 2-type cell-representing factor IL-4 and transcription factor GATA-3 (panels G and H).
FIG. 3 shows the interference effects of different interference fragments siRNA-BRAF-972, siRNA-BRAF-1341 and siRNA-BRAF-1845/siRNA-NC and OE-BRAF. As can be seen from panel B, the interference effect of the siRNA-BRAF-1341 fragment is the best.
FIG. 4 is a graph showing the differentiation of mouse spleen-initiated CD4+ T cells after transfection of OE-BRAF and siRNA-BRAF-1341. As can be seen from FIG. 4, after transfection of siRNA-BRAF-1341, the levels of the Th1 type cytokine IFN-gamma and transcription factor T-bet mRNA are significantly increased (panels C and D), while the levels of the Th2 type cytokine IL-4 and transcription factor GATA-3mRNA are significantly decreased (panels G and H), after transfection of OE-BRAF, the levels of the Th1 type cytokine IFN-gamma and transcription factor T-bet mRNA are significantly decreased (panels A and B), while the levels of the Th2 type cytokine IL-4 and transcription factor GATA-3mRNA are significantly increased (panels E and F).
FIG. 5 shows the result of the function recovery of miR-378a-5p target gene BRAF. As can be seen from fig. 5, after co-transfection of miR-378a-5p and BRAF in mouse spleen-initialized CD4+ T cells, the promotion of differentiation of miR-378a-5 p-initiated CD4+ T cells toward Th1 direction can be restored by BRAF.
5、Western blot
(1) SDS-PAGE gels were prepared. Formulated as in table 8.
TABLE 8SDS-PAGE gel composition
(2) Adding samples according to the sequence of a marker, a sample 1 and a sample 2, wherein the voltage is set to be 80V, when bromophenol blue runs to about 1 cm below the separation gel, the voltage is adjusted to be 120V, continuing electrophoresis for about 2 hours, and when bromophenol blue runs to the bottom of the glass plate, stopping electrophoresis;
(3) Transferring membrane, namely firstly placing PVDF membrane in methanol to activate for about 8-10 minutes, then immersing a membrane transferring clamp, filter paper and the like in membrane transferring liquid pre-cooled in advance, peeling SDS-PAGE gel, clamping the membrane transferring clamp according to the sequence of a red plate, a sponge cushion, the filter paper, the PVDF membrane, the gel, the filter paper, the sponge cushion and a blackboard, placing the membrane transferring clamp in a membrane transferring groove, switching on a power supply of an electrophoresis apparatus, setting constant current 250mA for 2 hours, and starting membrane transferring;
(4) Sealing, namely preparing 5% skimmed milk, placing the skimmed milk on a shaking table at normal temperature, and sealing for 2 hours at 65 rpm/min;
(5) Washing the membrane with TBST, at 110rpm/min, repeating for three times each for 6 min;
(6) An antibody is prepared in advance, a PVDF membrane is placed in the prepared antibody, and the PVDF membrane is incubated by a shaking table at 4 ℃ overnight;
(7) Washing the membrane, namely recovering the primary antibody, and washing the membrane by TBST three times for 6min each time;
(8) Secondary antibody incubation, namely preparing the secondary antibody in advance, placing the PVDF film into the prepared antibody, and incubating for 2 hours on a shaking table at normal temperature;
(9) Washing the membrane, namely recovering the secondary antibody, and washing the membrane by TBST for three times, wherein each time is 6min;
(10) And (3) exposure, namely preparing ECL chemiluminescent liquid, photographing through an imaging system, storing a result and analyzing data.
The results are shown in fig. 6 and 7:
as can be seen from FIG. 6, the transfection of miR-378a-5p mimics can promote the expression of the Th1 cell representative factor IFN-gamma and inhibit the expression of the Th2 cell representative factor IL-4, and the transfection of miR-378a-5p inhibitor can inhibit the expression of the Th1 cell representative factor IFN-gamma and promote the expression of the Th2 cell representative factor IL-4.
As can be seen from FIG. 7, after transfection of siRNA-BRAF-1341, the expression of the Th1 type cytokine IFN-gamma protein is obviously increased, while the expression of the Th2 type cytokine IL-4 is obviously decreased, and after transfection of OE-BRAF, the expression of the Th1 type cytokine IFN-gamma protein is obviously decreased, while the expression of the Th2 type cytokine IL-4 is obviously increased. The above findings indicate that BRAF inhibits the differentiation of mouse spleen naive CD4+ T cells in Th1 direction, promoting their differentiation in Th2 direction.
6. Flow cytometry
(1) 1 Μl (24 well plate) cell stimulation cocktail and protein transport inhibitor (500×) was added before harvesting the cells for 5h;
(2) The cell quantity of each tube is regulated to be 1 multiplied by 106, and the tube is resuspended by buffer 2;
(3) Surface dyeing, namely adding PerCP-Cy5.5-CD3 and APC-CD4 into the mixture, mixing the mixture uniformly by vortex, and incubating the mixture for 30min at 4 ℃ in a dark place;
(4) Washing, namely adding 1mL buffer 2,350xg,4 ℃ into each tube, and centrifuging for 8min;
(5) Fixing, namely adding 600 mu L of 4% paraformaldehyde into each tube, and fixing for 15min at normal temperature in a dark place;
(6) Washing, namely adding 1mL buffer 2,350xg,4 ℃ into each tube, and centrifuging for 8min;
(7) 1mL buffer 3 is added to each tube, and the membrane is broken overnight at 4 ℃ in the dark;
(8) Intracellular staining, namely adding 100 mu L buffer 3 into each tube for re-suspension after centrifugation for 8min at 350xg and 4 ℃ in the next day, adding 2 mu L PE-IFN-gamma or PE-IL-4, and incubating for 30min at 4 ℃ in the dark;
(9) Washing, namely adding 1mL buffer 2,350xg,4 ℃ into each tube, and centrifuging for 8min;
(10) And (3) loading the sample, namely, re-suspending the sample by using about 350 mu L buffer 2, and loading the sample after filtration.
The results are shown in FIG. 8-FIG. 10:
as can be seen from FIG. 8, the transfection of miR-378a-5p mimics can promote the expression of the Th1 cell representative factor IFN-gamma and inhibit the expression of the Th2 cell representative factor IL-4, and the transfection of miR-378a-5p inhibitor can inhibit the expression of the Th1 cell representative factor IFN-gamma and promote the expression of the Th2 cell representative factor IL-4.
As can be seen from FIG. 9, after transfection of siRNA-BRAF-1341, the expression of the Th1 type cytokine IFN-gamma protein is obviously increased, while the expression of the Th2 type cytokine IL-4 is obviously decreased, and after transfection of OE-BRAF, the expression of the Th1 type cytokine IFN-gamma protein is obviously decreased, while the expression of the Th2 type cytokine IL-4 is obviously increased. The above findings also demonstrate that BRAF inhibits differentiation of mouse spleen naive CD4+ T cells in Th1 direction, promoting differentiation in Th2 direction.
FIG. 10 is a result of the recovery of the function of the miR-378a-5p target gene BRAF. As can be seen from fig. 10, after co-transfection of miR-378a-5p and BRAF in mouse spleen-initialized CD4+ T cells, the promotion of differentiation of the initialized CD4+ T cells to Th1 direction caused by miR-378a-5p can be restored by BRAF.
Example 2
In the embodiment, the targeting relationship between miR-378a-5p and BRAF is detected through a double-luciferase reporter gene.
Referring to the Dual-Luciferase ReporterAssay System kit from Promega, the specific steps are as follows:
(1) 293T cells and plasmids of interest, which are divided into 96-well plates, are prepared in advance for transfection, preferably until the cell density reaches 50% -70%.
(2) Mu.L of DMEM was thoroughly mixed with 0.16. Mu.g of Dlk1-3UTR target plasmid and 5pmol of mmu-miR-378a-5p/NC, and then left at room temperature (solution A), after which 10. Mu.L of DMEM was thoroughly mixed with 0.3. Mu.L of transfection reagent (0.8 mg/ml) (solution B), and left at room temperature for 5min.
(3) And (3) fully and uniformly mixing the solution A and the solution B, and standing at room temperature for 20min.
(4) Cells were exchanged for fresh medium prior to transfection, and the transfection mixture was added to mix. Culturing at 37deg.C with 5% CO2.
(5) Fresh medium was exchanged after 6h of transfection and cell detection was collected after 48h of transfection.
(6) The ratio of the expression quantity of the Renilla luciferase to the firefly luciferase is the relative activity of the Renilla luciferase, namely the activity of the corresponding target gene (three repeats).
Experimental results:
Construction of the BRAF wild-type (wt) 3' UTR and 3' UTR containing the sequence mutation of the predicted binding site into psiCHECK-2, by double luciferase reporter assay, it was found that the BRAF wild-type 3' UTR region was regulated by miR-378a-5p, whereas the mutant was not regulated by miR-378a-5 p. As shown in fig. 11.
Example 3
This example demonstrates the expression of miR-378a-5p and BRAF after rEg.P29 immunization of mice.
(1) Expression and purification of rEg.P29. The recombinant strain preserved in the laboratory in earlier stage is selected, induced and amplified for culture, and then purified by utilizing an affinity chromatography method.
(2) The experimental animals were grouped, immunized and obtained by randomly dividing 18 female Balb/c mice of 6-8 weeks of age into three groups (6 in each group) of PBS group, adjuvant group and rEg.P29+ adjuvant group. The immunization protocol was PBS group (100. Mu.L PBS), adjuvant group (50. Mu.L PBS+50. Mu.L adjuvant), rEg.P29+adjuvant group (20. Mu.g.P29+50. Mu.L PBS+50 MLFCA), immunization 2 times, 1 week apart, two times each with three subcutaneous injections into the abdomen, wherein the first adjuvant was Freund's complete adjuvant and the second adjuvant was Freund's incomplete adjuvant. After 1 week of the second immunization, the magnetic beads sorted spleen CD4+ T cells and RNA and protein were extracted.
(3) RNA expression conditions of miR-378a-5P and BRAF are detected by using a qRT-PCR technology, and BRAF protein expression conditions are detected by using a Western blot technology, so that the result is shown in figure 12, compared with PBS and an adjuvant group, miR-378a-5P expression in a P29+ adjuvant group is obviously increased, and the expression level of BRAF is obviously reduced.
The foregoing description of the preferred embodiments of the invention is not intended to be limiting, but rather is intended to cover all modifications, equivalents, and alternatives falling within the spirit and principles of the invention.

Claims (10)

Translated fromChinese
1.miR-378a-5p在促进初始化CD4+T细胞向Th1方向分化中的应用。1. Application of miR-378a-5p in promoting the differentiation of initialized CD4+ T cells towards Th1.2.根据权利要求1所述的应用,其特征在于,所述miR-378a-5p的核苷酸序列为CUCCUGACUCCAGGUCCUGUGU。2. The use according to claim 1, characterized in that the nucleotide sequence of miR-378a-5p is CUCCUGACUCCAGGUCCUGUGU.3.miR-378a-5p模拟物在制备棘球蚴病预防或治疗药物中的应用。3. Application of miR-378a-5p mimics in the preparation of drugs for the prevention or treatment of echinococcosis.4.根据权利要求3所述的应用,其特征在于,所述miR-378a-5p模拟物为双链:正义链序列为:CUCCUGACUCCAGGUCCUGUGU,反义链序列为:ACAGGACCUGGAGUCAGGAGUU。4. The use according to claim 3, characterized in that the miR-378a-5p mimic is double-stranded: the sense strand sequence is: CUCCUGACUCCAGGUCCUGUGU, and the antisense strand sequence is: ACAGGACCUGGAGUCAGGAGUU.5.一种预防棘球蚴病的药物,其特征在于,其活性成分包括miR-378a-5p模拟物。5. A drug for preventing echinococcosis, characterized in that its active ingredient includes a miR-378a-5p mimic.6.根据权利要求5所述的药物,其特征在于,所述miR-378a-5p模拟物为双链:正义链序列为:CUCCUGACUCCAGGUCCUGUGU,反义链序列为:ACAGGACCUGGAGUCAGGAGUU。6. The drug according to claim 5, characterized in that the miR-378a-5p mimic is double-stranded: the sense strand sequence is: CUCCUGACUCCAGGUCCUGUGU, and the antisense strand sequence is: ACAGGACCUGGAGUCAGGAGUU.7.根据权利要求5或6所述的药物,其特征在于,所述药物的剂型为注射剂。7. The medicine according to claim 5 or 6, characterized in that the dosage form of the medicine is an injection.8.一种治疗棘球蚴病的药物,其特征在于,其活性成分包括miR-378a-5p模拟物。8. A drug for treating echinococcosis, characterized in that its active ingredient includes a miR-378a-5p mimic.9.根据权利要求8所述的药物,其特征在于,所述miR-378a-5p模拟物为双链:正义链序列为:CUCCUGACUCCAGGUCCUGUGU,反义链序列为:ACAGGACCUGGAGUCAGGAGUU。9. The drug according to claim 8, characterized in that the miR-378a-5p mimic is double-stranded: the sense strand sequence is: CUCCUGACUCCAGGUCCUGUGU, and the antisense strand sequence is: ACAGGACCUGGAGUCAGGAGUU.10.根据权利要求8或9所述的药物,其特征在于,所述药物的剂型为注射剂。10. The medicine according to claim 8 or 9, characterized in that the dosage form of the medicine is an injection.
CN202410868909.2A2024-07-012024-07-01 Application of miR-378a-5p in promoting the differentiation of initialized CD4+T cells into Th1PendingCN119082017A (en)

Priority Applications (1)

Application NumberPriority DateFiling DateTitle
CN202410868909.2ACN119082017A (en)2024-07-012024-07-01 Application of miR-378a-5p in promoting the differentiation of initialized CD4+T cells into Th1

Applications Claiming Priority (1)

Application NumberPriority DateFiling DateTitle
CN202410868909.2ACN119082017A (en)2024-07-012024-07-01 Application of miR-378a-5p in promoting the differentiation of initialized CD4+T cells into Th1

Publications (1)

Publication NumberPublication Date
CN119082017Atrue CN119082017A (en)2024-12-06

Family

ID=93699844

Family Applications (1)

Application NumberTitlePriority DateFiling Date
CN202410868909.2APendingCN119082017A (en)2024-07-012024-07-01 Application of miR-378a-5p in promoting the differentiation of initialized CD4+T cells into Th1

Country Status (1)

CountryLink
CN (1)CN119082017A (en)

Similar Documents

PublicationPublication DateTitle
EP3299023A1 (en)Low-oxygen-treated mesenchymal stem cell and use thereof
JP2022521997A (en) Use of circular RNA in the preparation of drugs to treat systemic lupus erythematosus
US20230272034A1 (en)T-cell receptor of hla-a11-restricted hepatitis b virus hbc141-151 epitope peptide, and application thereof
CN108753773A (en)Interfere CD19-CAR-T cells and its application of IFN-gama expression
CN102002493B (en)Application of small RNA-326 in preparation of medicament
CN113046301A (en)Model for human nasal mucosa epithelial cell inflammation induced by combination of tumor suppressor M and lipopolysaccharide, preparation method and application
CN119082017A (en) Application of miR-378a-5p in promoting the differentiation of initialized CD4+T cells into Th1
CN107217071A (en)A kind of adenovirus of recombinant rat phospholipase C γ 2, construction method and its application
CN114917325B (en)Application of human soluble TIM-4 protein in preparation of antitumor drugs
CN119331908A (en) CAR-T cell preparation method and product
CN118480131A (en)Chimeric antigen receptor immune cell specifically targeting FAP+ fibroblast and application thereof
CN110129272A (en) PK-15 cell line stably expressing MAP3K8 protein and its construction and application
CN108948163A (en)Queensland nut plant alexin and its application
Zhang et al.CCR3 gene knockout inhibits proliferation, differentiation, and migration of eosinophils in allergic rhinitis model mice
CN105779480A (en)Recombinant adeno-associated virus carrier carrying multi-site mutant EGFR (Epidermal Growth Factor Receptor) novel antigenic gene as well as construction method and application of recombinant adeno-associated virus carrier
CN111000839A (en)Use of dimethylarginine and its derivatives for inhibiting T, B cell proliferation
CN119925572B (en)Application of TMEM171 protein in preparation of antiviral drugs
CN114807233B (en)Macrophage specificity USP13 overexpression recombinant adeno-associated virus and application thereof
CN101270363B (en)DNA vaccine carrier of single-chain RNA expression with immune activation function and uses thereof
CN114058581B (en) Application of miR-126a-5p in CD4+ T cell differentiation
CN114480309B (en) ShRNA lentivirus inhibiting ALKBH1 expression and its preparation and application
CN117624340B (en)T Cell Receptor (TCR) recognizing human Hepatitis B Virus (HBV) antigen and use thereof
CN107058230B (en)Preparation method of T lymphocyte for silencing T cell antigen receptor
CN118389442A (en)Recombinant mesenchymal stem cells, preparation method and application
CN120192922A (en) In vitro induced tolerant dendritic cells and preparation method and application thereof

Legal Events

DateCodeTitleDescription
PB01Publication
PB01Publication
SE01Entry into force of request for substantive examination
SE01Entry into force of request for substantive examination

[8]ページ先頭

©2009-2025 Movatter.jp