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Adenovirus-mediated P311 inhibits TGF-β1-induced epithelial-mesenchymal transition in NRK-52E cells via TGF-β1-Smad-ILK pathway.
Biosci Trends. 2015 Oct; 9(5):299-306.BT

Abstract

P311, a highly conserved 8-kDa intracellular protein, has been indicated as an important factor in myofibroblast transformation and in the progression of fibrosis. In the present study, we constructed a recombinant adenovirus vector of p311 (called Ad-P311) and transferred it into rat renal proximal tubular epithelial cells (NRK-52E) to explore the effect of P311 on epithelial-mesenchymal transition (EMT) of NRK-52E cells induced by TGF-β1 and to elucidate its underlying mechanism against EMT. After successfully construction of Ad-P311 and transfer into NRK-52E cells, the proliferation and growth of P311-expressing cells was detected by MTT assay. TGF-β1 was used to induce NRK-52E cells and Western blot analysis was used to examine the EMT markers (E-cadherin and α-smooth muscle actin (α-SMA)), signal transducers (p-Smad2/3 and Smad7). Integrin Linked Kinase (ILK) as a key intracellular mediator that controls TGF-β1-induced-EMT was also assayed by Western blot analysis. The results showed that P311 transfection could significantly inhibit the proliferation and growth of TGF-β1 induced NRK-52E cells. The results also showed that TGF-β1 could induce EMT in NRK-52E cells through Smad-ILK signaling pathway with an increase in α-SMA, pSmad2/3 and ILK expression, and a decrease in E-cadherin and Smad7 expression. However, P311 efficiently blocked Smad-ILK pathway activation and attenuated all these EMT changes induced by TGF-β1. These findings suggest that P311 might be involved in the pathogenesis of renal fibrosis by inhibiting the EMT process via TGF-β1-Smad-ILK pathway. P311 might be a novel target for the control of renal fibrosis and the progression of CKD.

Authors+Show Affiliations

Department of Traditional Chinese Medicine, Shandong Provincial Hospital affiliated to Shandong University.No 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

26559022

Citation

Qi, Fanghua, et al. "Adenovirus-mediated P311 Inhibits TGF-β1-induced Epithelial-mesenchymal Transition in NRK-52E Cells Via TGF-β1-Smad-ILK Pathway." Bioscience Trends, vol. 9, no. 5, 2015, pp. 299-306.
Qi F, Cai P, Liu X, et al. Adenovirus-mediated P311 inhibits TGF-β1-induced epithelial-mesenchymal transition in NRK-52E cells via TGF-β1-Smad-ILK pathway. Biosci Trends. 2015;9(5):299-306.
Qi, F., Cai, P., Liu, X., Peng, M., & Si, G. (2015). Adenovirus-mediated P311 inhibits TGF-β1-induced epithelial-mesenchymal transition in NRK-52E cells via TGF-β1-Smad-ILK pathway. Bioscience Trends, 9(5), 299-306. https://doi.org/10.5582/bst.2015.01129
Qi F, et al. Adenovirus-mediated P311 Inhibits TGF-β1-induced Epithelial-mesenchymal Transition in NRK-52E Cells Via TGF-β1-Smad-ILK Pathway. Biosci Trends. 2015;9(5):299-306. PubMed PMID: 26559022.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Adenovirus-mediated P311 inhibits TGF-β1-induced epithelial-mesenchymal transition in NRK-52E cells via TGF-β1-Smad-ILK pathway. AU - Qi,Fanghua, AU - Cai,Pingping, AU - Liu,Xiang, AU - Peng,Min, AU - Si,Guomin, PY - 2015/11/13/entrez PY - 2015/11/13/pubmed PY - 2016/9/8/medline SP - 299 EP - 306 JF - Bioscience trends JO - Biosci Trends VL - 9 IS - 5 N2 - P311, a highly conserved 8-kDa intracellular protein, has been indicated as an important factor in myofibroblast transformation and in the progression of fibrosis. In the present study, we constructed a recombinant adenovirus vector of p311 (called Ad-P311) and transferred it into rat renal proximal tubular epithelial cells (NRK-52E) to explore the effect of P311 on epithelial-mesenchymal transition (EMT) of NRK-52E cells induced by TGF-β1 and to elucidate its underlying mechanism against EMT. After successfully construction of Ad-P311 and transfer into NRK-52E cells, the proliferation and growth of P311-expressing cells was detected by MTT assay. TGF-β1 was used to induce NRK-52E cells and Western blot analysis was used to examine the EMT markers (E-cadherin and α-smooth muscle actin (α-SMA)), signal transducers (p-Smad2/3 and Smad7). Integrin Linked Kinase (ILK) as a key intracellular mediator that controls TGF-β1-induced-EMT was also assayed by Western blot analysis. The results showed that P311 transfection could significantly inhibit the proliferation and growth of TGF-β1 induced NRK-52E cells. The results also showed that TGF-β1 could induce EMT in NRK-52E cells through Smad-ILK signaling pathway with an increase in α-SMA, pSmad2/3 and ILK expression, and a decrease in E-cadherin and Smad7 expression. However, P311 efficiently blocked Smad-ILK pathway activation and attenuated all these EMT changes induced by TGF-β1. These findings suggest that P311 might be involved in the pathogenesis of renal fibrosis by inhibiting the EMT process via TGF-β1-Smad-ILK pathway. P311 might be a novel target for the control of renal fibrosis and the progression of CKD. SN - 1881-7823 UR - https://www.unboundmedicine.com/medline/citation/26559022/Adenovirus_mediated_P311_inhibits_TGF_β1_induced_epithelial_mesenchymal_transition_in_NRK_52E_cells_via_TGF_β1_Smad_ILK_pathway_ L2 - https://dx.doi.org/10.5582/bst.2015.01129 DB - PRIME DP - Unbound Medicine ER -