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Erbin inhibits TGF-β1-induced EMT in renal tubular epithelial cells through an ERK-dependent pathway.
J Mol Med (Berl). 2012 May; 90(5):563-74.JM

Abstract

Epithelial-to-mesenchymal transition (EMT) plays a crucial role in the progression of renal interstitial fibrosis, which finally leads to renal failure. Erbin, a member of LAP family, is recently reported to inhibit Smads and ERK pathway which are two important types of intracellular signaling involved in TGF-β1-induced EMT. However, the role of Erbin in the regulation of EMT and the underlying mechanisms remain to be fully understood. To that end, we aimed to evaluate the expression of Erbin in renal interstitial fibrosis and the potential role of Erbin in tubular EMT stimulated by TGF-β1. In this study we demonstrated that the expression of Erbin was upregulated in the tubular epithelia of 5/6-nephrectomized rats. We also showed here that TGF-β1 upregulated Erbin expression in NRK52E cells during their EMT phenotype acquisition. Importantly, elevated expression of Erbin inhibited ERK signaling and partial reversed EMT stimulated by TGF-β1. In the mean time, reducing Erbin expression enhanced ERK phosphorylation, promoted the E-cadherin suppression, and induced α-SMA expression and fibronection secretion in response to TGF-β1, which could be rescued if cells were treated with the inhibitor of MEK1/2 U0126. However, in the absence of TGF-β1, Erbin failed to affect ERK activation and EMT process. These results suggest that Erbin is a negative feedback molecule induced by TGF-β1 and inhibits TGF-β1-induced EMT via ERK signaling pathway.

Authors+Show Affiliations

Division of Nephrology, Department of Internal Medicine, Tongji Hospital, Tongji Medical College, Wuhan, Hubei, People's Republic of China.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

22116522

Citation

Zhou, Qiaodan, et al. "Erbin Inhibits TGF-β1-induced EMT in Renal Tubular Epithelial Cells Through an ERK-dependent Pathway." Journal of Molecular Medicine (Berlin, Germany), vol. 90, no. 5, 2012, pp. 563-74.
Zhou Q, Zeng R, Xu C, et al. Erbin inhibits TGF-β1-induced EMT in renal tubular epithelial cells through an ERK-dependent pathway. J Mol Med (Berl). 2012;90(5):563-74.
Zhou, Q., Zeng, R., Xu, C., Liu, L., Chen, L., Kou, P., Pei, G., Bai, S., Zhang, Y., Li, C., Rong, S., Han, M., & Xu, G. (2012). Erbin inhibits TGF-β1-induced EMT in renal tubular epithelial cells through an ERK-dependent pathway. Journal of Molecular Medicine (Berlin, Germany), 90(5), 563-74. https://doi.org/10.1007/s00109-011-0833-4
Zhou Q, et al. Erbin Inhibits TGF-β1-induced EMT in Renal Tubular Epithelial Cells Through an ERK-dependent Pathway. J Mol Med (Berl). 2012;90(5):563-74. PubMed PMID: 22116522.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Erbin inhibits TGF-β1-induced EMT in renal tubular epithelial cells through an ERK-dependent pathway. AU - Zhou,Qiaodan, AU - Zeng,Rui, AU - Xu,Chuou, AU - Liu,Lili, AU - Chen,Lin, AU - Kou,Pei, AU - Pei,Guangchang, AU - Bai,Shoujun, AU - Zhang,Yamin, AU - Li,Caixia, AU - Rong,Song, AU - Han,Min, AU - Xu,Gang, Y1 - 2011/11/25/ PY - 2011/05/28/received PY - 2011/10/31/accepted PY - 2011/10/17/revised PY - 2011/11/26/entrez PY - 2011/11/26/pubmed PY - 2012/11/2/medline SP - 563 EP - 74 JF - Journal of molecular medicine (Berlin, Germany) JO - J Mol Med (Berl) VL - 90 IS - 5 N2 - Epithelial-to-mesenchymal transition (EMT) plays a crucial role in the progression of renal interstitial fibrosis, which finally leads to renal failure. Erbin, a member of LAP family, is recently reported to inhibit Smads and ERK pathway which are two important types of intracellular signaling involved in TGF-β1-induced EMT. However, the role of Erbin in the regulation of EMT and the underlying mechanisms remain to be fully understood. To that end, we aimed to evaluate the expression of Erbin in renal interstitial fibrosis and the potential role of Erbin in tubular EMT stimulated by TGF-β1. In this study we demonstrated that the expression of Erbin was upregulated in the tubular epithelia of 5/6-nephrectomized rats. We also showed here that TGF-β1 upregulated Erbin expression in NRK52E cells during their EMT phenotype acquisition. Importantly, elevated expression of Erbin inhibited ERK signaling and partial reversed EMT stimulated by TGF-β1. In the mean time, reducing Erbin expression enhanced ERK phosphorylation, promoted the E-cadherin suppression, and induced α-SMA expression and fibronection secretion in response to TGF-β1, which could be rescued if cells were treated with the inhibitor of MEK1/2 U0126. However, in the absence of TGF-β1, Erbin failed to affect ERK activation and EMT process. These results suggest that Erbin is a negative feedback molecule induced by TGF-β1 and inhibits TGF-β1-induced EMT via ERK signaling pathway. SN - 1432-1440 UR - https://www.unboundmedicine.com/medline/citation/22116522/Erbin_inhibits_TGF_β1_induced_EMT_in_renal_tubular_epithelial_cells_through_an_ERK_dependent_pathway_ L2 - https://antibodies.cancer.gov/detail/CPTC-MAP2K1-1 DB - PRIME DP - Unbound Medicine ER -