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Fluorofenidone suppresses epithelial-mesenchymal transition and the expression of connective tissue growth factor via inhibiting TGF-beta/Smads signaling in human proximal tubular epithelial cells.
Pharmazie. 2011 Dec; 66(12):961-7.P

Abstract

OBJECTIVES

The present study was designed to investigate the potential effects and mechanism of fluorofenidone (AKF-PD) on transforming growth factor beta1 (TGF-beta1)-induced tubular epithelial-mesenchymal transition (EMT) and the expression of connective tissue growth factor (CTGF) in human proximal tubular epithelial cells.

METHODS

HK-2 cells were pretreated with AKF-PD, pirfenidone (PFD), Losartan, and SB431542 (an inhibitor of TGF-beta type I receptor). The pretreated HK-2 cells were subsequently co-treated with TGF-beta1 (5 ng/ml). The morphological changes of HK-2 cells were observed under an inverted microscope. Expression of alpha-SMA was detected by Western blot and immunofluorescence. The protein expression of ZO-1, fibronectin, CTGF, phosphorylated Smad2 (p-Smad2) and phosphorylated Smad3 (p-Smad3) were evaluated by Western blot.

RESULTS

Through down-regulation of p-Smad2 and p-Smad3 proteins, AKF-PD significantly inhibited protein expression of alpha-SMA, fibronectin, and CTGF. Meanwhile, the depressed ZO-1 expression and morphological changes induced by TGF-beta1 were attenuated by AKF-PD.

CONCLUSION

AKF-PD acts as an anti-fibrotic agent through blocking TGF-beta/Smads signaling and consequently inhibits TGF-beta1-induced EMT and CTGF expression in human proximal tubular epithelial cells.

Authors+Show Affiliations

Division of Nephrology, Xiangya Hospital, Central South University, Changsha, Hunan.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 available

Pub Type(s)

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

Language

eng

PubMed ID

22312703

Citation

Yuan, Qiongjing, et al. "Fluorofenidone Suppresses Epithelial-mesenchymal Transition and the Expression of Connective Tissue Growth Factor Via Inhibiting TGF-beta/Smads Signaling in Human Proximal Tubular Epithelial Cells." Die Pharmazie, vol. 66, no. 12, 2011, pp. 961-7.
Yuan Q, Wang L, Zhang F, et al. Fluorofenidone suppresses epithelial-mesenchymal transition and the expression of connective tissue growth factor via inhibiting TGF-beta/Smads signaling in human proximal tubular epithelial cells. Pharmazie. 2011;66(12):961-7.
Yuan, Q., Wang, L., Zhang, F., Wang, R., Fu, X., Peng, Z., Ning, W., Hu, G., Wang, Z., & Tao, L. (2011). Fluorofenidone suppresses epithelial-mesenchymal transition and the expression of connective tissue growth factor via inhibiting TGF-beta/Smads signaling in human proximal tubular epithelial cells. Die Pharmazie, 66(12), 961-7.
Yuan Q, et al. Fluorofenidone Suppresses Epithelial-mesenchymal Transition and the Expression of Connective Tissue Growth Factor Via Inhibiting TGF-beta/Smads Signaling in Human Proximal Tubular Epithelial Cells. Pharmazie. 2011;66(12):961-7. PubMed PMID: 22312703.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Fluorofenidone suppresses epithelial-mesenchymal transition and the expression of connective tissue growth factor via inhibiting TGF-beta/Smads signaling in human proximal tubular epithelial cells. AU - Yuan,Qiongjing, AU - Wang,Linghao, AU - Zhang,Fangfang, AU - Wang,Rui, AU - Fu,Xiao, AU - Peng,Zhangzhe, AU - Ning,Wangbin, AU - Hu,Gaoyun, AU - Wang,Zhaohe, AU - Tao,Lijian, PY - 2012/2/9/entrez PY - 2012/2/9/pubmed PY - 2012/3/21/medline SP - 961 EP - 7 JF - Die Pharmazie JO - Pharmazie VL - 66 IS - 12 N2 - OBJECTIVES: The present study was designed to investigate the potential effects and mechanism of fluorofenidone (AKF-PD) on transforming growth factor beta1 (TGF-beta1)-induced tubular epithelial-mesenchymal transition (EMT) and the expression of connective tissue growth factor (CTGF) in human proximal tubular epithelial cells. METHODS: HK-2 cells were pretreated with AKF-PD, pirfenidone (PFD), Losartan, and SB431542 (an inhibitor of TGF-beta type I receptor). The pretreated HK-2 cells were subsequently co-treated with TGF-beta1 (5 ng/ml). The morphological changes of HK-2 cells were observed under an inverted microscope. Expression of alpha-SMA was detected by Western blot and immunofluorescence. The protein expression of ZO-1, fibronectin, CTGF, phosphorylated Smad2 (p-Smad2) and phosphorylated Smad3 (p-Smad3) were evaluated by Western blot. RESULTS: Through down-regulation of p-Smad2 and p-Smad3 proteins, AKF-PD significantly inhibited protein expression of alpha-SMA, fibronectin, and CTGF. Meanwhile, the depressed ZO-1 expression and morphological changes induced by TGF-beta1 were attenuated by AKF-PD. CONCLUSION: AKF-PD acts as an anti-fibrotic agent through blocking TGF-beta/Smads signaling and consequently inhibits TGF-beta1-induced EMT and CTGF expression in human proximal tubular epithelial cells. SN - 0031-7144 UR - https://www.unboundmedicine.com/medline/citation/22312703/Fluorofenidone_suppresses_epithelial_mesenchymal_transition_and_the_expression_of_connective_tissue_growth_factor_via_inhibiting_TGF_beta/Smads_signaling_in_human_proximal_tubular_epithelial_cells_ L2 - https://antibodies.cancer.gov/detail/CPTC-TGFB1-1 DB - PRIME DP - Unbound Medicine ER -