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microRNA related to autoimmune disease and application thereof

An autoimmune and miRNA-23 technology, applied in allergic diseases, DNA/RNA fragments, metabolic diseases, etc., can solve problems such as unclear miRNA

Active Publication Date: 2013-10-30
SHANGHAI INST OF BIOLOGICAL SCI CHINESE ACAD OF SCI
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  • Summary
  • Abstract
  • Description
  • Claims
  • Application Information

AI Technical Summary

Problems solved by technology

[0006] So far, little is known about the relationship between autoimmune diseases and microRNAs in this field. Although some miRNAs, such as miR-155, miR-146a and miR-326, mainly regulate the pathogenesis of autoimmune diseases by affecting T cell function, the original How miRNAs in bit cells function in autoimmune disease is not well understood

Method used

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  • microRNA related to autoimmune disease and application thereof
  • microRNA related to autoimmune disease and application thereof
  • microRNA related to autoimmune disease and application thereof

Examples

Experimental program
Comparison scheme
Effect test

Embodiment 1

[0179] Example 1 The expression of miRNA-23b is generally down-regulated in autoimmune diseases

[0180] In order to determine whether a ubiquitous miRNA plays a role in the inflammatory injury site of various autoimmune diseases, this embodiment takes RA and SLE patients and related mice (CIA corresponds to RA, MRL / lpr corresponds to SLE, EAE corresponds to MS ) of inflamed tissues were subjected to comparative miRNA microarray analysis. The human miRNA chip contains 754 miRNAs, and the detection samples include the synovial tissues of RA patients and control groups, and the kidney biopsy tissues of SLE patients and control groups; the mouse miRNA chip contains 641 miRNAs, and detects CIA and control mice respectively. Joint samples, kidney tissue from female MRL / lpr and control mice and spinal cord specimens from EAE and control mice.

[0181] The detection results are as follows: Compared with the control group, in all autoimmune disease samples, including RA, SLE, CIA, MR...

Embodiment 2I

[0184] Example 2 IL-17 down-regulates the expression of miR-23b

[0185] A common feature of inflammatory autoimmune diseases is local chronic inflammation, which is manifested in the increased production of inflammatory factors such as TNFα and IL-1β, both of which can regulate the expression level of miRNA in cell culture. MiR-23b-3p was significantly decreased in local inflammatory tissues of RA and SLE patients, while inflammatory factors including TNFα, IL-1β, IL-17, IL-6 and IFNγ were significantly increased in these tissues ( figure 2 c, 2d).

[0186] The inventors performed a linear correlation analysis on the transcript level of miR-23b-3p and the above cytokines, and the results showed that the expression level of miR-23b-3p was inversely correlated with the level of IL-17, both in RA patients and their controls group (P figure 2 a, 2b), suggesting that the expression of IL-17 in inflammatory tissues may regulate the downregulation of miR-23b-3p.

[0187] To furth...

Embodiment 3

[0189] Example 3 MiR-23 family inhibits signaling pathways and gene expression mediated by inflammatory factors

[0190] The activation of NF-κB signaling pathway mediated by inflammatory factors plays an important role in the pathogenesis of autoimmune diseases. The inventors found that overexpression of miR-23b-3p significantly inhibited the activation of NF-κB mediated by TNFα and IL-1β as well as the activation of NF-κB mediated by IL-17 ( image 3 a, image 3 b). Next, the inventors in human FLS cells ( image 3 c), mouse primary kidney cells ( image 3 d) and mouse primary astrocytes ( image 3 In e), it was found that miR-23b-3p mimics could inhibit the induced expression of inflammatory factors (TNFα, IL-1β and IL-17) to their downstream inflammatory genes such as IC and IL-6, while miR-23b-3p inhibitors This effect is enhanced. The above results indicated that miR-23b-3p inhibited the signaling pathway and gene expression mediated by inflammatory factors.

[01...

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Abstract

Provided is an auto-immune disease-related microRNA. In particular, provided is the miR-23b generally down-regulated in the partially inflamed tissue, and further provided are members of the miR-23 family capable of inhibiting the occurrence and development of auto-immune disease after the members are introduced, comprising miR-23a, miR-23b and miR-23C. Also provided is the use of the microRNA in the treatment and prevention of auto-immune disease. The expression of miR-23b is regulated by IL-17, and targets the genes of TAB2 and TAB3, etc., in the signal pathway of inflammatory factors; by inhibiting the expression of TAB2 and TAB3, miR-23b can inhibit the occurrence and development of auto-immune disease and significantly relieve the symptoms and development of the disease.

Description

technical field [0001] The invention belongs to the field of biotechnology and medicine, in particular, the invention relates to microRNAs related to autoimmune diseases and applications thereof. Background technique [0002] Autoimmune diseases are a kind of diseases caused by the body's immune response to self-antigens, resulting in damage to its own tissues. It is generally believed that abnormal inflammatory reactions occur at the tissue damage caused by various autoimmune diseases, such as rheumatoid arthritis ( rheumatoid arthritis, RA), multiple sclerosis (multiple sclerosis, MS) and systemic lupus erythematosus (systemic lupus erythematosus, SLE). RA is characterized by synovial inflammation accompanied by articular bone and cartilage damage, MS is an inflammatory lesion characterized by demyelination of the central nervous system, and SLE is an immune complex deposition. Chronic activation of the immune system results in multisystem autoimmune disease, often accomp...

Claims

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Application Information

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Patent Type & Authority Applications(China)
IPC IPC(8): A61K48/00A61K45/00A61K31/7088C12N15/113C12Q1/68A61P37/02A61P17/06A61P17/00A61P1/04A61P3/10A61P19/02A61P19/00A61P25/00
CPCA61K31/7105C12N2310/141C12N15/113A61K31/713A61P1/04A61P3/10A61P17/00A61P17/06A61P19/00A61P19/02A61P25/00A61P37/02A61P37/06G01N33/5023G01N2800/24
Inventor 钱友存沈南朱书潘文
Owner SHANGHAI INST OF BIOLOGICAL SCI CHINESE ACAD OF SCI
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