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miR29

作者其他创作

大纲/内容

Tet1

mir29 0.99

miR-124-3p.1 0.97

Tet2

mir29 0.99

let-7-5p/98-5p 0.96

let-7d--tet2-0.96

miR-125a-5p 0.91

Tet3

mir29 0.99

let-7-5p/98-5p 0.99

let-7d--tet3-0.99

在小鼠哮喘模型中，抑制TH2反应中的IL-13（JACI）

miR-124-3p.1 0.99

miR-125a-5P 0.81

miR-29

子主题

文献

IL-6负调节TGF-β和miR-29

Zhang, Y., et al. (2016). "Deletion of interleukin-6 alleviated interstitial fibrosis in streptozotocin-induced diabetic cardiomyopathy of mice through affecting TGFbeta1 and miR-29 pathways." Sci Rep 6: 23010.

miR-29 inhibitor (AMO29)

miR-29a F: 5′ -CCGTAGCACCATCTGAAATC-3′

miR-29a R: 5′ -GTATCCAGTGCGTGTCGTG-3′

U6 F: 5′ - GCTTCGGCAGCACATATACTAAAAT -3′

U6 R: 5′ - CGCTTCACGAATTTGCGTGTCAT -3′

miR-29 family (miR-29a, miR-29b and miR-29c) can directly repress Tet1 expression.

Cui, Y., et al. (2016). "miR-29 regulates Tet1 expression and contributes to early differentiation of mouse ESCs." Oncotarget.

Erratum Negative feedback of miR-29 family TET1 involves in hepatocellular cancer."

Lin, L. L., et al. (2015). "Erratum to: Negative feedback of miR-29 family TET1 involves in hepatocellular cancer." Med Oncol 32(3): 39.

Lin, L. L., et al. (2014). "Negative feedback of miR-29 family TET1 involves in hepatocellular cancer." Med Oncol 31(12): 291.

miR-29 family, target gene IFN-gamma

Yi, Z. J., et al. (2013). "[Expression and bioinformatic analysis of miR-29 family, target gene IFN-gamma in CD4(+) T cells from subjects with latent tuberculosis infection]." Zhonghua Yu Fang Yi Xue Za Zhi 47(7): 632-636.

子主题

Yang, T., et al. (2013). "miR-29 mediates TGFbeta1-induced extracellular matrix synthesis through activation of PI3K-AKT pathway in human lung fibroblasts." J Cell Biochem 114(6): 1336-1342.

GATA3能激活microRNA-29b

GATA3 suppresses metastasis and modulates the tumour microenvironment by regulating microRNA-29b expression

文章思路参考

mir155-RA

Elmesmari, A., et al. (2016). "MicroRNA-155 regulates monocyte chemokine and chemokine receptor expression in Rheumatoid Arthritis." Rheumatology (Oxford).

在con/RA/RA SF的PBMC-CD14+中用PCR发现miR155在炎症中上调

在RA/RA SF中，探讨miR155与风湿标志物ACPA、多种症状评分的相关性（不一定有统计学差异，but also a data）

in vitro： RA的PB CD14+的单核细胞体外过表达miR-155 in RA monocytes stimulated the production of CCL3, CCL4, CCL5 and CCL8; upregulated CCR7 expression; and downregulated CCR2.

Taqman low-density arrays for chemokine and chemokine

receptor expression 芯片

in vitro : 小鼠的骨髓细胞，干扰miR155后，对比表面趋化因子等的表达

miR124

2016 Oct 4;7:406. eCollection 2016. IF=5.69

miRNA-124 in Immune System and Immune Disorders.

Qin Z1, Wang PY1, Su DF1, Liu X1.

Author information

1Department of Pharmacology, School of Pharmacy, Second Military Medical University , Shanghai , China.

2015 Sep;25(5):784-9. doi: 10.3109/14397595.2015.1023887. Epub 2015 Jul 20. IF=1.8

MicroRNA-124 involves in ankylosing spondylitis by targeting ANTXR2.

Xia Y1, Chen K, Zhang MH, Wang LC, Ma CY, Lin YL, Zhao YR.

Abstract

OBJECTIVES:

A recent genome-wide association study or GWAS identified that anthrax roxin receptor 2 (ANTXR2) was one of the risk loci for ankylosing spondylitis (AS). Previous study also showed that ANTXR2 could potentially affect new bone formation. This study aimed to investigate the possible mechanisms of ANTXR2 involved in AS pathogenesis.

METHODS:

The expression level of ANTXR2 and miR-124 in peripheral blood was detected by quantitative real-time polymerase chain reaction or qRT-PCR. ANTXR2 was predicted to be a target gene of miR-124 by TargetScan, which was confirmed by luciferase reporter assays. Western blot analysis was used to further investigate the effect of miR-124 on c-Jun N-terminal kinase (JNK) activation and evaluate the activated status of autophagy.

RESULTS:

We evidenced that ANTXR2 was downregulated and miR-124 was upregulated in peripheral blood from AS patients. Intriguingly, miR-124 targeted ANTXR2 and overexpression of miR-124 in Jurkat cells notably inhibited ANTXR2 expression. ANTXR2 inhibition by miR-124promoted JNK activation and induced autophagy.

CONCLUSIONS:

Our results suggested that miR-124 might induce autophagy to participate in AS by targeting ANTXR2, which might be implicated in pathological process of AS.

2016 Oct 5. [Epub ahead of print]

Nicotine protects against DSS colitis through regulating microRNA-124 and STAT3.

Qin Z1, Wan JJ1, Sun Y1, Wu T2, Wang PY1, Du P2, Su DF3, Yang Y4, Liu X5.

2016 Oct 27:0. [Epub ahead of print]

Cocaine-mediated downregulation of microglial miR-124 expression involves promoter DNA methylation.

Guo ML1, Periyasamy P1, Liao K1, Kook YH1, Niu F1, Callen SE1, Buch S1.

2016;45(1):1-10. doi: 10.3109/08820139.2015.1085390. Epub 2015 Dec 23. 1.78

Role of miR-146a in Enforcing Effect of Specific Immunotherapy on Allergic Rhinitis.

Liu HJ1,2, Zhang AF2, Zhao N2, Li XZ1.

模型方法参考

Allergic rhinitis (AR) is one of the common disorders in airway allergic inflammation. The pathogenesis of AR is unclear. It is accepted that immune deregulation is associated with the pathogenesis of AR. Recent reports suggest that a large number of micro RNAs (miR) can regulate immune functions. This study aims to investigate the role of miR-146a in an enforcing immunotherapy of AR. In this study, a mouse AR model was created. The levels of miR-146a in the mouse nasal mucosa were assessed by real time RT-PCR. A specific immunotherapy was performed in AR mice. The results showed that the AR mice had an AR-like inflammation in the nasal mucosa. Compared with naïve mice, markedly lower levels of miR-146a were detected in AR mice. The co-administration with miR-146a significantly enforced the effect of ovalbumin (OVA)-specific immunotherapyon inhibition of AR inflammation in the nasal mucosa. Further analysis showed that miR-146a induced transforming growth factor-β in dendritic cells; the latter induced naïve CD4(+) T cells to differentiate into regulatory T cells. In conclusion, miR-146a can enforce OVA-specific immunotherapy via inducing antigen-specific regulatory T cells. miR-146a may have therapeutic potential to be used in the immunotherapy of allergic diseases.

经典文献

2013 Sep 23;210(10):1993-2010. doi: 10.1084/jem.20121200. Epub 2013 Sep 16.

VEGF controls lung Th2 inflammation via the miR-1-Mpl (myeloproliferative leukemia virus oncogene)-P-selectin axis.

Takyar S1, Vasavada H, Zhang JG, Ahangari F, Niu N, Liu Q, Lee CG, Cohn L, Elias JA.

mir干预鼻部炎症的研究经典问下 -from pro li

2015 Apr;15(2):156-62. doi: 10.1097/ACI.0000000000000147. IF =2.7

Role of microRNAs in allergic asthma: present and future.

Perry MM1, Adcock IM, Chung KF.

2014 May;133(5):1429-38, 1438.e1-7. doi: 10.1016/j.jaci.2013.11.008. Epub 2013 Dec 24.

MicroRNA-155 is essential for T(H)2-mediated allergen-induced eosinophilic inflammation in the lung.

Malmhäll C1, Alawieh S1, Lu Y1, Sjöstrand M1, Bossios A1, Eldh M1, Rådinger M2.

To investigate a role for miR-155 in the regulation of allergic inflammation in vivo, we used miR-155 knockout (KO) and wild-type (WT) mice sensitized and exposed to ovalbumin.

RESULTS:

miR-155 deficiency resulted in diminished eosinophilic inflammation and mucus hypersecretion in the lungs of allergen-sensitized and allergen-challenged mice compared with WT control animals. This was supported by a reduction in T(H)2 cell numbers and airway T(H)2 cytokine levels and complete abrogation of allergen-induced airway eotaxin-2/CCL24 and periostin levels in miR-155 KO mice. Intranasal instillation of eotaxin-2/CCL24 before allergen challenge partially restored airway eosinophilia in miR-155 KO mice, and adoptive transfer of CD4(+) T cells resulted in a similar degree of airway eosinophilia in miR-155 KO and WT mice. Furthermore, the transcription factor PU.1, a negative regulator of T(H)2 cytokine production, was upregulated in the airways of allergen-challenged miR-155 KO mice compared with WT mice.

CONCLUSIONS:

Our data provides evidence that miR-155 contributes to the regulation of allergic airway inflammation by modulating T(H)2 responses through the transcription fac

2016 May 12;17(5). pii: E716. doi: 10.3390/ijms17050716. 刘争教授的综述，好好看

MicroRNA in United Airway Diseases.

Liu Z1, Zhang XH2, Callejas-Díaz B3, Mullol J4.

The concept of united airway diseases (UAD) has received increasing attention in recent years. Sustained and increased inflammation is a common feature of UAD, which is inevitably accompanied with marked gene modification and tight gene regulation. However, gene regulation in the common inflammatory processes in UAD remains unclear. MicroRNA (miRNA), a novel regulator of gene expression, has been considered to be involved in many inflammatory diseases. Although there are an increasing number of studies of miRNAs in inflammatory upper and lower airway diseases, few miRNAs have been identified that directly link the upper and lower airways. In this article, therefore, we reviewed the relevant studies available in order to improve the understanding of the roles of miRNAs in the interaction and pathogenesis of UAD.