ArticleJournal of the American Society of Nephrology : JASN2016
MicroRNA-196a/b Mitigate Renal Fibrosis by Targeting TGF-β Receptor 2.
Article in Journal of the American Society of Nephrology : JASN, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 66 citations in OpenAlex.
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- Type 2 Innate Lymphoid Cell (Ilc2)-Deficient Mice Are Transcriptionally Constrained DuringPathogens (Basel, Switzerland) · 2025Article
- ELABELA-derived peptide ELA13 attenuates kidney fibrosis by inhibiting the Smad and ERK signaling pathways.Journal of Zhejiang University. Science. B · 2024Article
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- Effect of extracellular vesicles derived from induced pluripotent stem cells on mesangial cells underwent a model of fibrosis in vitro.Scientific reports · 2023Article
- Complement induces podocyte pyroptosis in membranous nephropathy by mediating mitochondrial dysfunction.Cell death & disease · 2022Article
- A Klotho-derived peptide protects against kidney fibrosis by targeting TGF-β signaling.Nature communications · 2022Article
- Novel Concepts in Systemic Sclerosis Pathogenesis: Role for miRNAs.Biomedicines · 2021Review
- MicroRNA-10 negatively regulates inflammation in diabetic kidney via targeting activation of the NLRP3 inflammasome.Molecular therapy : the journal of the American Society of Gene Therapy · 2021Article
- Integrin β3 Induction Promotes Tubular Cell Senescence and Kidney Fibrosis.Frontiers in cell and developmental biology · 2021Article
- MicroRNA-302b mitigates renal fibrosis via inhibiting TGF-β/Smad pathway activation.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2021Article
- MicroRNA regulation postbleomycin due to the R213G extracellular superoxide dismutase variant is predicted to suppress inflammatory and immune pathways.Physiological genomics · 2020Article
- Targeting the progression of chronic kidney disease.Nature reviews. Nephrology · 2020Review
- Circular RNA circ_0003204 inhibits proliferation, migration and tube formation of endothelial cell in atherosclerosis via miR-370-3p/TGFβR2/phosph-SMAD3 axis.Journal of biomedical science · 2020Article
- Emerging role of miRNAs in renal fibrosis.RNA biology · 2020Review
- miR-20a-5p/TGFBR2 Axis Affects Pro-inflammatory Macrophages and Aggravates Liver Fibrosis.Frontiers in oncology · 2020Article
- MicroRNA-140-5p Mediates Renal Fibrosis Through TGF-β1/Smad Signaling Pathway by Directly Targeting TGFBR1.Frontiers in physiology · 2020Article
- Identification of cell and disease specific microRNAs in glomerular pathologies.Journal of cellular and molecular medicine · 2019Article
- C3a and suPAR drive versican V1 expression in tubular cells of focal segmental glomerulosclerosis.JCI insight · 2019Article
- Signal regulatory protein α protects podocytes through promoting autophagic activity.JCI insight · 2019Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Organ-specific microRNAs have essential roles in maintaining normal organ function. However, the microRNA profile of the kidney and the role of microRNAs in modulating renal function remain undefined. We performed an unbiased assessment of the genome-wide microRNA expression profile in 14 mouse organs using Solexa deep sequencing and found that microRNA-196a (miR-196a) and miR-196b are selectively expressed in kidney, with 74.37% of mouse total miR-196a and 73.19% of mouse total miR-196b distributed in the kidneys. We confirmed the predominant expression of miR-196a/b in mouse and human kidney, particularly in the glomeruli and tubular epithelium, by quantitative RT-PCR and in situ hybridization assays. During unilateral ureteral obstruction (UUO)-induced mouse renal fibrosis, renal miR-196a/b levels rapidly decreased. Elevation of renal miR-196a/b expression by hydrodynamic-based delivery of a miR-196a/b-expressing plasmid before or shortly after UUO significantly downregulated profibrotic proteins, including collagen 1 and α-smooth muscle actin, and mitigated UUO-induced renal fibrosis. In contrast, depletion of renal miR-196a/b by miR-196a/b antagomirs substantially aggravated UUO-induced renal fibrosis. Mechanistic studies further identified transforming growth factor beta receptor II (TGFβR2) as a common target of miR-196a and miR-196b. Decreasing miR-196a/b expression in human HK2 cells strongly activated TGF-β-Smad signaling and cell fibrosis; whereas increasing miR-196a/b levels in mouse primary cultured tubular epithelial cells inhibited TGF-β-Smad signaling. In the UUO model, miR-196a/b silenced TGF-β-Smad signaling, decreased the expression of collagen 1 and α-smooth muscle actin, and attenuated renal fibrosis. Our findings suggest that elevating renal miR-196a/b levels may be a novel therapeutic strategy for treating renal fibrosis.
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