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Evodiamine might inhibit TGF-beta1-induced epithelial-mesenchymal transition in NRK52E cells via Smad and PPAR-gamma pathway.
Cell Biol Int. 2014 Jul; 38(7):875-80.CB

Abstract

Epithelial-mesenchymal transition (EMT) is involved in renal tubulointerstitial fibrosis. Transforming growth factor (TGF)-beta1 is the main inducer of EMT. Phosphorylation of Smad proteins and PPAR-gamma activation are required for the process of TGF-beta1-induced EMT. Evodiamine possesses anti-inflammatory, anti-obesity, anti-cancer, and anti-nociceptive effects. We have examined the effects of evodiamine in EMT induced by TGF-beta1 and the role of Smad and PPAR-gamma signal pathway in rat renal proximal tubular epithelial (NRK52E) cells in vitro. E-cadherin, alpha-smooth muscle actin (SMA), Smad 2 and PPAR-gamma mRNA and protein expressions were detected by real-time PCR and Western blot, respectively. NRK52E treated with TGF-beta1 for 48 h induced EMT, as evidenced by loss of E-cadherin and de novo expression of alpha-SMA. EMT was almost completely blocked by evodiamine and rosiglitazone. TGF-beta1 significantly increased Smad 2 expression and decreased PPAR-gamma expression in NRK52E cells compared with the control group, while evodiamine and rosiglitazone almost reversed these effects. These observations suggest that evodiamine and rosiglitazone inhibit TGF-beta1-induced EMT in NRK52E cells. Smad 2 and PPAR-gamma signal pathway might participate in the effects of evodiamine and rosiglitazone in EMT induced by TGF-beta1.

Authors+Show Affiliations

Department of Nephrology, Hainan General Hospital, Haikou, Hainan, 570311, China.No affiliation info availableNo affiliation info available

Pub Type(s)

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

Language

eng

PubMed ID

24604887

Citation

Wei, Jiali, et al. "Evodiamine Might Inhibit TGF-beta1-induced Epithelial-mesenchymal Transition in NRK52E Cells Via Smad and PPAR-gamma Pathway." Cell Biology International, vol. 38, no. 7, 2014, pp. 875-80.
Wei J, Li Z, Yuan F. Evodiamine might inhibit TGF-beta1-induced epithelial-mesenchymal transition in NRK52E cells via Smad and PPAR-gamma pathway. Cell Biol Int. 2014;38(7):875-80.
Wei, J., Li, Z., & Yuan, F. (2014). Evodiamine might inhibit TGF-beta1-induced epithelial-mesenchymal transition in NRK52E cells via Smad and PPAR-gamma pathway. Cell Biology International, 38(7), 875-80. https://doi.org/10.1002/cbin.10270
Wei J, Li Z, Yuan F. Evodiamine Might Inhibit TGF-beta1-induced Epithelial-mesenchymal Transition in NRK52E Cells Via Smad and PPAR-gamma Pathway. Cell Biol Int. 2014;38(7):875-80. PubMed PMID: 24604887.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Evodiamine might inhibit TGF-beta1-induced epithelial-mesenchymal transition in NRK52E cells via Smad and PPAR-gamma pathway. AU - Wei,Jiali, AU - Li,Zhuori, AU - Yuan,Feng, Y1 - 2014/03/18/ PY - 2013/10/14/received PY - 2014/02/07/accepted PY - 2014/3/8/entrez PY - 2014/3/8/pubmed PY - 2015/1/17/medline KW - PPAR-gamma KW - Smad KW - TGF-beta1 KW - epithelial-mesenchymal transition KW - evodiamine SP - 875 EP - 80 JF - Cell biology international JO - Cell Biol Int VL - 38 IS - 7 N2 - Epithelial-mesenchymal transition (EMT) is involved in renal tubulointerstitial fibrosis. Transforming growth factor (TGF)-beta1 is the main inducer of EMT. Phosphorylation of Smad proteins and PPAR-gamma activation are required for the process of TGF-beta1-induced EMT. Evodiamine possesses anti-inflammatory, anti-obesity, anti-cancer, and anti-nociceptive effects. We have examined the effects of evodiamine in EMT induced by TGF-beta1 and the role of Smad and PPAR-gamma signal pathway in rat renal proximal tubular epithelial (NRK52E) cells in vitro. E-cadherin, alpha-smooth muscle actin (SMA), Smad 2 and PPAR-gamma mRNA and protein expressions were detected by real-time PCR and Western blot, respectively. NRK52E treated with TGF-beta1 for 48 h induced EMT, as evidenced by loss of E-cadherin and de novo expression of alpha-SMA. EMT was almost completely blocked by evodiamine and rosiglitazone. TGF-beta1 significantly increased Smad 2 expression and decreased PPAR-gamma expression in NRK52E cells compared with the control group, while evodiamine and rosiglitazone almost reversed these effects. These observations suggest that evodiamine and rosiglitazone inhibit TGF-beta1-induced EMT in NRK52E cells. Smad 2 and PPAR-gamma signal pathway might participate in the effects of evodiamine and rosiglitazone in EMT induced by TGF-beta1. SN - 1095-8355 UR - https://www.unboundmedicine.com/medline/citation/24604887/Evodiamine_might_inhibit_TGF_beta1_induced_epithelial_mesenchymal_transition_in_NRK52E_cells_via_Smad_and_PPAR_gamma_pathway_ L2 - https://doi.org/10.1002/cbin.10270 DB - PRIME DP - Unbound Medicine ER -