ArticleThe Journal of biological chemistry2011
Response gene to complement 32 is essential for fibroblast activation in renal fibrosis.
Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 36 citations in OpenAlex.
- Article
- Single-Cell RNA-Sequencing Analyses Identify APLNR, INS-IGF2, RGCC Genes May Be Involved in the Pathogenesis of Systemic Sclerosis Skin.Clinical, cosmetic and investigational dermatology · 2024Article
- Effect of Semaglutide and Empagliflozin on Pulmonary Structure and Proteomics in Obese Mice.Diabetes, metabolic syndrome and obesity : targets and therapy · 2024Article
- Pumping the Brakes on Pulmonary Fibrosis: A New Role for Regulator of Cell Cycle.American journal of respiratory cell and molecular biology · 2022Article
- Regulator of Cell Cycle Protein (RGCC/RGC-32) Protects against Pulmonary Fibrosis.American journal of respiratory cell and molecular biology · 2022Article
- ADAM17 knockdown mitigates while ADAM17 overexpression aggravates cardiac fibrosis and dysfunctionFrontiers in pharmacology · 2022Article
- RGCC balances self-renewal and neuronal differentiation of neural stem cells in the developing mammalian neocortex.EMBO reports · 2021Article
- ND-13, a DJ-1-Derived Peptide, Attenuates the Renal Expression of Fibrotic and Inflammatory Markers Associated with Unilateral Ureter Obstruction.International journal of molecular sciences · 2020Article
- From cirrhosis to hepatocellular carcinoma: An investigation into hepatitis C viral oncogenesis.Hepatology forum · 2020Article
- Molecular mechanism for the multiple sclerosis risk variant rs17594362.Human molecular genetics · 2019Article
- RGC-32 and diseases: the first 20 years.Immunologic research · 2019Review
- Response Gene to Complement 32 Maintains Blood Pressure Homeostasis by Regulating α-Adrenergic Receptor Expression.Circulation research · 2018Article
- RGC32 Promotes Bleomycin-Induced Systemic Sclerosis in a Murine Disease Model by Modulating Classically Activated Macrophage Function.Journal of immunology (Baltimore, Md. : 1950) · 2018Article
- Response Gene to Complement 32 in Vascular Diseases.Frontiers in cardiovascular medicine · 2018Review
- Specific and spatial labeling of P0-Cre versus Wnt1-Cre in cranial neural crest in early mouse embryos.Genesis (New York, N.Y. : 2000) · 2017Article
- RGC-32 Promotes Th17 Cell Differentiation and Enhances Experimental Autoimmune Encephalomyelitis.Journal of immunology (Baltimore, Md. : 1950) · 2017Article
- RGC32 induces epithelial-mesenchymal transition by activating the Smad/Sip1 signaling pathway in CRC.Scientific reports · 2017Article
- Response gene to complement 32 regulates the G2/M phase checkpoint during renal tubular epithelial cell repair.Cellular & molecular biology letters · 2016Article
- RGC-32 Deficiency Protects against Hepatic Steatosis by Reducing Lipogenesis.The Journal of biological chemistry · 2015Article
- RGC32 deficiency protects against high-fat diet-induced obesity and insulin resistance in mice.The Journal of endocrinology · 2015Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
Response gene to complement 32 (RGC-32) is a downstream target of transforming growth factor-β (TGF-β). TGF-β is known to play a pathogenic role in renal fibrosis. In this study, we investigated RGC-32 function in renal fibrosis following unilateral ureteral obstruction (UUO) in mice, a model of progressive tubulointerstitial fibrosis. RGC-32 is normally expressed only in blood vessels of mouse kidney. However, UUO induces RGC-32 expression in renal interstitial cells at the early stage of kidney injury, suggesting that RGC-32 is involved in interstitial fibroblast activation. Indeed, expression of smooth muscle α-actin (α-SMA), an indicator of fibroblast activation, is limited to the interstitial cells at the early stage, and became apparent later in both interstitial and tubular cells. RGC-32 knockdown by shRNA significantly inhibits UUO-induced renal structural damage, α-SMA expression and collagen deposition, suggesting that RGC-32 is essential for the onset of renal interstitial fibrosis. In vitro studies indicate that RGC-32 mediates TGF-β-induced fibroblast activation. Mechanistically, RGC-32 interacts with Smad3 and enhances Smad3 binding to the Smad binding element in α-SMA promoter as demonstrated by DNA affinity assay. In the chromatin setting, Smad3, but not Smad2, binds to α-SMA promoter in fibroblasts. RGC-32 appears to be essential for Smad3 interaction with the promoters of fibroblast activation-related genes in vivo. Functionally, RGC-32 is crucial for Smad3-mediated α-SMA promoter activity. Taken together, we identify RGC-32 as a novel fibrogenic factor contributing to the pathogenesis of renal fibrosis through fibroblast activation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.