ArticleAmerican journal of translational research2015
Norcantharidin inhibits renal interstitial fibrosis by downregulating PP2Ac expression.
Article in American journal of translational research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 16 citations in OpenAlex.
- Norcantharidin attenuates amiodarone-induced pulmonary fibrosis via modulating miRNA-30a/GSK-3β/β-catenin and oxidative-inflammatory pathways.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Nr4a1 promotes renal interstitial fibrosis by regulating the p38 MAPK phosphorylation.Molecular medicine (Cambridge, Mass.) · 2023Article
- Norcantharidin ameliorates the development of murine lupus via inhibiting the generation of IL-17 producing cells.Acta pharmacologica Sinica · 2022Article
- Role of protein phosphatase 2A in kidney disease (Review).Experimental and therapeutic medicine · 2021Review
- PP2Acα promotes macrophage accumulation and activation to exacerbate tubular cell death and kidney fibrosis through activating Rap1 and TNFα production.Cell death and differentiation · 2021Article
- Protein Phosphatase 2A Inhibiting β-Catenin Phosphorylation Contributes Critically to the Anti-renal Interstitial Fibrotic Effect of Norcantharidin.Inflammation · 2020Article
- PP2Ac Modulates AMPK-Mediated Induction of Autophagy inInternational journal of molecular sciences · 2019Article
- Effect of norcantharidin on the proliferation, apoptosis, and cell cycle of human mesangial cells.Renal failure · 2017Article
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Authors and funding
13 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Norcantharidin (NCTD) has been proven to be able to attenuate renal interstitial fibrosis, but the exact molecular mechanism is still unknown. This study investigated the relationship between the anti-fibrotic effect of NCTD and its inhibition on PP2Ac expression. Here, PP2Ac was found to be positively correlated with extracellular matrix accumulation in the rat unilateral ureteral obstruction (UUO) model. Additional experiments showed that the PP2A inhibitor (okadaic acid) can ameliorate renal interstitial fibrosis by inhibiting the expression of fibronectin (FN) and collagen I (Col-I) and reversing tubular epithelial-to-mesenchymal transition in vivo and in vitro. In vitro experiments also demonstrated that ectopic over-expression of PP2Ac has a profibrotic effect in HK-2 cells. Moreover, NCTD was able to downregulate PP2Ac expression, decrease FN, Col-I, α-SMA expression, and increase E-cadherin expression in a dose-dependent manner both in vivo and in vitro. In particular, it was demonstrated that NCTD induced no evident changes in the expression of FN, Col-I, α-SMA and E-cadherin in HK-2 cells after PP2Ac was knocked down by shRNA. These results indicated that NCTD exerts an anti-fibrosis effect via inhibition of PP2Ac expression. Thus, PP2Ac could be a promising target for intervention in renal interstitial fibrosis.
Indexed as
Identifiers
26807168PMC4697700W2418129810What OpenQuestion holds
Registered trials
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