ArticleActa pharmacologica Sinica2016
Histone deacetylase inhibitors attenuate P-aIgA1-induced cell proliferation and extracellular matrix synthesis in human renal mesangial cells in vitro.
Article in Acta pharmacologica Sinica, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 23 citations in OpenAlex.
- Integrative bioinformatics analysis unveils hub transcription factors and their interacting drugs in immunoglobulin A nephropathy: Implications for pathogenesis and treatments.Journal, genetic engineering & biotechnology · 2025Article
- Histone deacetylases and their inhibitors in kidney diseases.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Review
- Epigenetic Regulation of EMP/EMT-Dependent Fibrosis.International journal of molecular sciences · 2024Review
- Molecular insight in intrarenal inflammation affecting four main types of cells in nephrons in IgA nephropathy.Frontiers in medicine · 2023Review
- Identification of key cuproptosis-related genes and their targets in patients with IgAN.BMC nephrology · 2022Article
- Molecular mechanisms of histone deacetylases and inhibitors in renal fibrosis progression.Frontiers in molecular biosciences · 2022Review
- Histone Acetylation and Modifiers in Renal Fibrosis.Frontiers in pharmacology · 2022Review
- Reduced fecal short-chain fatty acids levels and the relationship with gut microbiota in IgA nephropathy.BMC nephrology · 2021Article
- Application of Histone Deacetylase Inhibitors in Renal Interstitial Fibrosis.Kidney diseases (Basel, Switzerland) · 2020Review
- Triptolide protects podocytes via autophagy in immunoglobulin A nephropathy.Experimental and therapeutic medicine · 2018Article
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Authors and funding
9 authors at 3 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
aimAberrantly glycosylated IgA1 is a key factor in the pathogenesis of IgA nephropathy (IgAN). In this study we investigated the effects of aggregated IgA1 derived from IgAN patients (P-aIgA1) on human renal mesangial cells (HMCs) and the anti-proliferative and antifibrotic effects of histone deacetylase (HDAC) inhibitors in vitro.
methodsThree types of IgA1 were prepared, ie, N-IgA1 (IgA1 from healthy volunteers), P-IgA1 (IgA1 from IgAN patients), and P-aIgA1 (aggregated IgA1 from IgAN patients). The isolated IgA1 was heated for thermal polymerization. The proliferation of human renal mesangial cells (HMCs) were assessed using MTT assay. The expression levels of relevant proteins were examined using immunoblotting assays or immunohistochemistry.
resultsP-aIgA1 (25-250 μg/mL) dose-dependently promoted the proliferation of HMCs, and markedly increased the protein levels of type I histone deacetylase (HDAC1, HDAC2 and HDAC8) in the cells. Both P-IgA1 and N-IgA1 were much weaker in stimulating cell proliferation and HDAC expression. P-aIgA1 (50 μg/mL) markedly increased the protein levels of Col1a1 and PAI-1, as well as pSmad2/3 and pStat3 in the cells. Pretreatment with the HDAC inhibitor trichostatin A (TSA, 250 nmol/L) or valproic acid (VPA, 400 μg/mL) partially reversed P-aIgA1-induced cell proliferation and extracellular matrix synthesis in HMCs.
conclusionP-aIgA1 produces pro-proliferative and profibrotic actions in HMCs via upregulating the expression of HDACs, and subsequently activating TGF-β/Smad2/3 and Jak2/Stat3 signaling pathways. Both VPA and TSA attenuate P-aIgA1-induced cell proliferation and fibrosis in HMCs.
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