Tags

Type your tag names separated by a space and hit enter

Tranilast attenuates TGF-β1-induced epithelial-mesenchymal transition in the NRK-52E cells.
Pak J Pharm Sci. 2014 Jan; 27(1):51-5.PJ

Abstract

We previously reported that tranilast can halt the pathogenesis of chronic cyclosporine nephrotoxicity in rats via the transforming growth factor-β (TGF-β) /Smad pathway, an important signaling system involved in epithelial-mesenchymal transition (EMT), but the exact underlying cellular mechanisms are not yet clear. Thus, by selecting TGF-β1-induced normal rat kidney proximal tubular epithelial cells (NRK-52E) as a model, we demonstrated potential modifying effect of tranilast on EMT-induced by TGF-β1 in vitro. NRK-52E cells were incubated with the blank vehicle (Dulbecco's modified Eagle's medium and F-12 (DMEM/F12) added with 10% fetal bovine serum (FBS)), 10 ng/ml TGF-β1 alone or together with 100, 200 or 400μM tranilast for 48 h after incubation in medium containing 1% FBS for 24 h. Cell morphological changes were observed to confirm occurrence of EMT. Protein expressions of two typical markers of EMT, E-cadherin and α-smooth muscle actin (α-SMA), were assessed by western blotting and flow cytometry, respectively. Our results showed that TGF-β1 induced spindle-like morphological transition, the loss of E-cadherin protein and upregulation of expression of α-SMA. However, the TGF-β1-produced changes in cellular morphology, E-cadherin and α-SMA were inversed by tranlilast in concentration-dependent manner. Our findings indicate that tranilast can directly inhibit EMT. Thus, it may be implied that regulation of EMT be the target to prevent renal tubulointerstitial fibrosis.

Authors+Show Affiliations

The Centre Laboratory, Kunshan First People's Hospital Affiliated to Jiangsu University, Kunshan, Jiangsu, China.Department of Nephrology, Kunshan First People's Hospital Affiliated to Jiangsu University, Kunshan, Jiangsu, China.The Centre Laboratory, Kunshan First People's Hospital Affiliated to Jiangsu University, Kunshan, Jiangsu, China.The Centre Laboratory, Kunshan First People's Hospital Affiliated to Jiangsu University, Kunshan, Jiangsu, China and The Emergency Center of Kunshan, Kunshan, Jiangsu, China.

Pub Type(s)

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

Language

eng

PubMed ID

24374452

Citation

Li, Sha-sha, et al. "Tranilast Attenuates TGF-β1-induced Epithelial-mesenchymal Transition in the NRK-52E Cells." Pakistan Journal of Pharmaceutical Sciences, vol. 27, no. 1, 2014, pp. 51-5.
Li SS, Liu QF, He AL, et al. Tranilast attenuates TGF-β1-induced epithelial-mesenchymal transition in the NRK-52E cells. Pak J Pharm Sci. 2014;27(1):51-5.
Li, S. S., Liu, Q. F., He, A. L., & Wu, F. R. (2014). Tranilast attenuates TGF-β1-induced epithelial-mesenchymal transition in the NRK-52E cells. Pakistan Journal of Pharmaceutical Sciences, 27(1), 51-5.
Li SS, et al. Tranilast Attenuates TGF-β1-induced Epithelial-mesenchymal Transition in the NRK-52E Cells. Pak J Pharm Sci. 2014;27(1):51-5. PubMed PMID: 24374452.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Tranilast attenuates TGF-β1-induced epithelial-mesenchymal transition in the NRK-52E cells. AU - Li,Sha-sha, AU - Liu,Qi-feng, AU - He,Ao-lin, AU - Wu,Fu-rong, PY - 2013/12/31/entrez PY - 2014/1/1/pubmed PY - 2014/3/1/medline SP - 51 EP - 5 JF - Pakistan journal of pharmaceutical sciences JO - Pak J Pharm Sci VL - 27 IS - 1 N2 - We previously reported that tranilast can halt the pathogenesis of chronic cyclosporine nephrotoxicity in rats via the transforming growth factor-β (TGF-β) /Smad pathway, an important signaling system involved in epithelial-mesenchymal transition (EMT), but the exact underlying cellular mechanisms are not yet clear. Thus, by selecting TGF-β1-induced normal rat kidney proximal tubular epithelial cells (NRK-52E) as a model, we demonstrated potential modifying effect of tranilast on EMT-induced by TGF-β1 in vitro. NRK-52E cells were incubated with the blank vehicle (Dulbecco's modified Eagle's medium and F-12 (DMEM/F12) added with 10% fetal bovine serum (FBS)), 10 ng/ml TGF-β1 alone or together with 100, 200 or 400μM tranilast for 48 h after incubation in medium containing 1% FBS for 24 h. Cell morphological changes were observed to confirm occurrence of EMT. Protein expressions of two typical markers of EMT, E-cadherin and α-smooth muscle actin (α-SMA), were assessed by western blotting and flow cytometry, respectively. Our results showed that TGF-β1 induced spindle-like morphological transition, the loss of E-cadherin protein and upregulation of expression of α-SMA. However, the TGF-β1-produced changes in cellular morphology, E-cadherin and α-SMA were inversed by tranlilast in concentration-dependent manner. Our findings indicate that tranilast can directly inhibit EMT. Thus, it may be implied that regulation of EMT be the target to prevent renal tubulointerstitial fibrosis. SN - 1011-601X UR - https://www.unboundmedicine.com/medline/citation/24374452/Tranilast_attenuates_TGF_β1_induced_epithelial_mesenchymal_transition_in_the_NRK_52E_cells_ DB - PRIME DP - Unbound Medicine ER -