ArticleJournal of molecular medicine (Berlin, Germany)2016
MAD2B promotes tubular epithelial-to-mesenchymal transition and renal tubulointerstitial fibrosis via Skp2.
Article in Journal of molecular medicine (Berlin, Germany), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 21 citations in OpenAlex.
- Hypoxia-preconditioned mesenchymal stromal cell-derived exosomes attenuate LPS-induced acute lung injury and early epithelial remodeling in mice: evidence for a miR-486a-5p-Skp2-GATA4 axis.Respiratory research · 2026Article
- Placenta mesenchymal stem cell-derived extracellular vesicles alleviate liver fibrosis by inactivating hepatic stellate cells through a miR-378c/SKP2 axis.Inflammation and regeneration · 2023Article
- Asparaginyl endopeptidase protects against podocyte injury in diabetic nephropathy through cleaving cofilin-1.Cell death & disease · 2022Article
- Metformin attenuates renal tubulointerstitial fibrosis via upgrading autophagy in the early stage of diabetic nephropathy.Scientific reports · 2021Article
- NCTD Prevents Renal Interstitial Fibrosis via Targeting Sp1/lncRNA Gm26669 Axis.International journal of biological sciences · 2021Article
- MAD2B-mediated cell cycle reentry of podocytes is involved in the pathogenesis of FSGS.International journal of biological sciences · 2021Article
- S-phase kinase-associated protein 2 is involved in epithelial-mesenchymal transition in methotrexate-resistant osteosarcoma cells.International journal of oncology · 2018Article
- HOXC8: a predictive glioma biomarker that induces epithelia-mesenchymal transition.Chinese neurosurgical journal · 2018Article
- MDM2 is implicated in high-glucose-induced podocyte mitotic catastrophe via Notch1 signalling.Journal of cellular and molecular medicine · 2017Article
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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
The mitotic arrest deficient protein MAD2B is a well-defined anaphase-promoting complex/cyclosome (APC/C) inhibitor and a small subunit of DNA polymerase zeta. It is critical for mitotic control and DNA repair. However, the pathological role of MAD2B in kidney diseases has not been fully elucidated. In the present study, we aim to explore the role of MAD2B in the pathogenesis of renal tubulointerstitial fibrosis (TIF) and the underlying mechanism. By immunofluorescence and immunohistochemistry, we found an obvious MAD2B enhancement in tubular area of TIF patients and unilateral ureteral obstruction (UUO) mice. In vitro, transforming growth factor-β1 (TGF-β1) induced a time-dependent MAD2B accumulation prior to tubular epithelial-to-mesenchymal transition (EMT) in a rat proximal tubular epithelial cell line, NRK-52E. Knocking down MAD2B using siRNA dramatically inhibited TGF-β1-induced tubular EMT process and subsequent extracellular matrix (ECM) production. We also found that Skp2, a confirmed APC/C-CDH1 substrate and E-cadherin destroyer, was increased in TGF-β1-treated proximal tubular epithelial cells, which could be blocked by MAD2B depletion. In addition, Skp2 expression was also found to be increased in the renal tubular area of UUO mice. Locally knocking down MAD2B expression in the renal cortex using lentiviral transfection inhibited Skp2 expression, tubular EMT, and subsequent ECM accumulation. Taken together, our data suggests a pro-fibrotic role of MAD2B in the pathogenesis of tubular EMT and TIF by inducing Skp2 expression. MAD2B might be a potential target of promising interventions for renal TIF. KEY MESSAGES: Renal fibrosis activates MAD2B expression in renal tubules of human and mouse. TGF-β1 contributes to MAD2B enhancement in rat tubular epithelial cells. MAD2B depletion alleviates renal tubulointerstitial fibrosis in vivo and in vitro. MAD2B promotes EMT transition in rat tubular epithelial cells by inducing Skp2.
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