MicroRNAs in Kidney Disease: An Emerging Understanding

Khella, Heba; Bakhet, Marize; Lichner, Zsuzsanna; Romaschin, Alexander D.; Jewett, Michael A.S.; Yousef, George M.

doi:10.1053/j.ajkd.2012.09.018

Cited by 41 publications

(34 citation statements)

References 108 publications

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“…18,31 Recently, the role of miRNAs in the kidney under homeostatic and pathologic conditions has emerged as a field of study of its own, 32,33 and although pilot studies have been undertaken to analyze the expression profile of miRNAs in patients with IgA nephropathy 21,34 and lupus nephritis, 35,36 their functional role in renal autoimmune disease is still largely unknown. 37 The first evidence for a functional role of miRNA in glomerular disease was derived from an elegant study showing that overexpression of miR-193a in mice resulted in podocyte injury and subsequent FSGS. 22 Moreover, we found that mice with miRNA-deficient CD4 + T cells (CD4-cre 3 Dicer fl/fl mice) 15,38 developed less severe GN (Supplemental Figure 2).…”

Section: Cd4mentioning

confidence: 99%

MicroRNA-155 Drives TH17 Immune Response and Tissue Injury in Experimental Crescentic GN

Krebs

Kapffer

Paust

et al. 2013

Journal of the American Society of Nephrology

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CD4+ T cells play a pivotal role in the pathogenesis of autoimmune disease, including human and experimental crescentic GN. Micro-RNAs (miRs) have emerged as important regulators of immune cell development, but the impact of miRs on the regulation of the CD4 + T cell immune response remains to be fully clarified. Here, we report that miR-155 expression is upregulated in the kidneys of patients with ANCAassociated crescentic GN and a murine model of crescentic GN (nephrotoxic nephritis). To elucidate the potential role of miR-155 in T cell-mediated inflammation, nephritis was induced in miR-155 2/2 and wildtype mice. The systemic and renal nephritogenic T H 17 immune response decreased markedly in nephritic miR-155 2/2 mice. Consistent with this finding, miR-155-deficient mice developed less severe nephritis, with reduced histologic and functional injury. Adoptive transfer of miR-155 2/2 and wild-type CD4 + T cells into nephritic recombination activating gene 1-deficient (Rag-1 2/2 ) mice showed the T cell-intrinsic importance of miR-155 for the stability of pathogenic T H 17 immunity. These findings indicate that miR-155 drives the T H 17 immune response and tissue injury in experimental crescentic GN and show that miR-155 is a potential therapeutic target in T H 17-mediated diseases.

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Section: Cd4mentioning

confidence: 99%

MicroRNA-155 Drives TH17 Immune Response and Tissue Injury in Experimental Crescentic GN

Krebs

Kapffer

Paust

et al. 2013

Journal of the American Society of Nephrology

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“…[26][27][28][29] The clinical relevance of genetic mutations affecting miRNA genes or miRNA binding sites has not been thoroughly investigated. However, some functional polymorphysms in miRNA genes have been discovered that might be relevant in the progression of diseases such as acute lymphoblastic leukemia 30 and diabetic retinopathy.…”

Section: Introductionmentioning

confidence: 99%

Role of MicroRNAs in the Trabecular Meshwork

González

Qiu

et al. 2014

Journal of Ocular Pharmacology and Therapeutics

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MicroRNAs (miRNAs) are now recognized as important post-transcriptional regulators of gene expression. MiRNAs are known to modulate cellular functions relevant to the normal and pathological physiology of the trabecular meshwork (TM) such as cell contraction and extracellular matrix turnover. There is also increasing evidence supporting the role of miRNAs in the pathogenesis of multiple diseases, and their potential value as both biomarkers of disease and therapeutic targets. However, compared with other tissues, our current knowledge regarding the roles played by miRNAs in the TM is still very limited. Here, we review the information currently available about miRNAs in the TM and discuss the main challenges and opportunities to incorporate the rapid progress in miRNA biology to the understanding of the normal and pathological physiology of the TM, and to develop novel clinical applications for diagnosis and therapy of high intraocular pressure.

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“…Des é tudes ré centes ont ainsi montré l'influence des phé nomè nes é pigé né tiques tels que l'hypermé thylation de gè nes spé cifiques comme RASAL-1, un inhibiteur de Ras, induisant la levé e d'inhibition de la prolifé ration des fibroblastes [22]. De plus, la dé couverte relativement ré cente de l'implication des microARN (miARN) dans le dé veloppement normal du rein [23] ou dans sa pathogenè se [24,25] a suscité une attention toute particuliè re sur le rôle majeur que les miARN jouent dans le dé veloppement de la fibrose ré nale.…”

Section: Fibrogenè Se Ré Naleunclassified