Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

MiRNAs expression in joint of Collagen-induced arthritis (CIA)

ABSTRACT: MicroRNAs (miRNAs) have been implicated as fine-tuning regulators controlling diverse biological processes at the level of posttranscriptional repression. Dysregulation of miRNAs has been described in various disease states, including inflammatory autoimmune diseases. By using high-throughput microRNA profiling analysis, we identified a series of miRNAs dysregulated in local inflammatory lesions of human patients with autoimmune diseases, as well as their relevant mouse models such as CIA. We isolated joint samples pooled from six CIA mice or from six naM-CM-/ve control mice. Total RNA was extracted for the TaqManM-BM-. Low Density Assay v3.0

ORGANISM(S): Mus musculus

SUBMITTER: Nan Shen

PROVIDER: E-GEOD-37422 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

The microRNA miR-23b suppresses IL-17-associated autoimmune inflammation by targeting TAB2, TAB3 and IKK-α.

Zhu Shu S Pan Wen W Song Xinyang X Liu Yan Y Shao Xinrui X Tang Yuanjia Y Liang Dong D He Dongyi D Wang Honglin H Liu Wenjun W Shi Yufang Y Harley John B JB Shen Nan N Qian Youcun Y

Nature medicine 20120701 7

Inflammatory cytokines such as interleukin-17 (IL-17) promote inflammatory autoimmune diseases. Although several microRNAs (miRNAs) have been shown to regulate autoimmune pathogenesis by affecting lymphocyte development and function, the role of miRNAs in resident cells present in inflammatory lesions remains unclear. Here we show that miR-23b is downregulated in inflammatory lesions of humans with lupus or rheumatoid arthritis, as well as in the mouse models of lupus, rheumatoid arthritis or mu ...[more]

PMID: 22660635

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Project description:Assessment of the extent to which the altered profiles of miRNA expression influence viral replication and latency, as well as the efficiency of host defenses, may be useful for understanding the basis of the HIV-1-related alterations in cellular physiology and immunologic control. To this end, three patient groups were enrolled. One group consisted of subjects who were classified as M-CM-)lite control long-term non-progressors (M-CM-)LTNP). A second study group was HIV-1-positive subjects, who were antiretroviral therapy naive. A third group was multiply exposed to HIV-1, but uninfected (MEU). This study allowed us to investigate the existence of a CD4+T- lymphocytes miRNAs signature able to discriminate among different stages of HIV-1 infection, and to evaluate whether the exposure to HIV-1 antigen is sufficient to change the miRNA profile. MicroRNAs inhibit HIV-1 expression by either modulating host innate immunity or by directly interfering with viral mRNAs. We evaluated the expression of 377 miRNAs in CD4+ T cells from HIV-1 M-CM-)lite LTNP (M-CM-)LTNP), naive and multiply exposed uninfected individuals (MEU) and we observed that the M-CM-)LTNP patients clustered with naive, whereas all MEU subjects grouped together. The discriminatory power of miRNAs showed that 21 miRNAs significantly differentiated M-CM-)LTNP from MEU and 23 miRNAs distinguished naive from MEU, while only 1 (miR-155) discriminated M-CM-)LTNP from naive. We proposed that miRNA expression may discriminate between HIV-1 infected and exposed but negative individuals. Analysis of miRNAs expression after exposure of healthy CD4+T cells to gp120 in vitro confirmed our hypothesis that a miRNA profile could be the result not only of a productive infection, but also of the exposure to HIV-1 products that leave a signature in immune cells. The comparison of normalized Dicer and Drosha expression in ex vivo and in vitro conditions revealed that these enzymes did not affect the change of miRNA profiles, supporting the existence of a Dicer-independent biogenesis pathway. We have compared miRNA profiles of CD4+ T-lymphocytes from 18 HIV-1-exposed subjects with healthy CD4+ T-lymphocytes following exposure to gp120 using a RT-qPCR assay.

Dataset Information

MiRNAs expression in joint of Collagen-induced arthritis (CIA)

Publications

The microRNA miR-23b suppresses IL-17-associated autoimmune inflammation by targeting TAB2, TAB3 and IKK-α.

Similar Datasets

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