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Beta-casomorphin-7 prevents epithelial-mesenchymal transdifferentiation of NRK-52E cells at high glucose level: Involvement of AngII-TGF-β1 pathway.
Peptides. 2015 Aug; 70:37-44.P

Abstract

BACKGROUND

Hyperglycemia is the most important risk factor in the progression of renal fibrosis in diabetic kidney. Based on previous studies, β-casomorphin-7 may exert anti-fibrotic activities in diabetic rats. However, the role of β-casomorphin-7 in the pathogenesis of renal tubulointerstitial fibrosis remains unclear. Thus, this study was designed to investigate the protective effect of β-casomorphin-7 on epithelial-mesenchymal transition (EMT) of NRK-52E cells treated under hyperglycemic condition and to explore the possible mechanism.

RESEARCH DESIGN AND METHODS

NRK-52E cells were cultured in high glucose (30 mM) for 3 days. Different concentrations of β-casomorphin-7, naloxone (antagonist of opioid receptor) and losartan (antagonist of angiotensin II type I receptor) were added in the culture. Expression of α-smooth muscle actin (α-SMA), E-cadherin, vimentin and cytokeratin19 mRNA were determined by real-time PCR. Protein levels of E-cadherin and α-SMA were analyzed by Western blotting. The concentrations of angiotensin (Ang) II and transforming growth factor β1 (TGF-β1) in the culture medium were determined.

RESULTS

High glucose-induced up-regulation of vimentin mRNA and α-SMA mRNA and protein were significantly inhibited by β-casomorphin-7. On the contrary, high glucose-induced down-regulation of cytokeratin19 mRNA and E-cad mRNA and protein was significantly reversed by β-casomorphin-7. β-casomorphin-7 significantly alleviate high glucose induced increase of AngII and TGF-β1 in the culture. Moreover, losartan significantly attenuated the expression of TGF-β1 and EMT of NRK-52E cells treated under hyperglycemic condition. But naloxone did not affect the EMT of NRK-52E cells treated by high glucose and β-casomorphin-7.

CONCLUSION

We demonstrate that β-casomorphin-7 has the potential to inhibit high glucose-induced renal proximal tubular EMT partly by modulating AngII-TGF-β1 pathway, but not by opioid receptor.

Authors+Show Affiliations

Key Lab of Animal Physiology and Biochemistry, Ministry of Agriculture, Nanjing Agriculture University, Nanjing, 210095, People's Republic of China; Key Lab of Human Function Genomics Jiangsu Province, Nanjing Medical University, Nanjing, 210029, People's Republic of China.Key Laboratory of Meat Processing and Quality Control, Ministry of Education, Nanjing Agricultural University, Nanjing 210095, People's Republic of China; Key Laboratory of Agricultural and Animal Products Processing and Quality Control, Ministry of Agriculture, Nanjing Agricultural University, Nanjing 210095, People's Republic of China.Key Lab of Animal Physiology and Biochemistry, Ministry of Agriculture, Nanjing Agriculture University, Nanjing, 210095, People's Republic of China.Key Lab of Animal Physiology and Biochemistry, Ministry of Agriculture, Nanjing Agriculture University, Nanjing, 210095, People's Republic of China.Key Lab of Animal Physiology and Biochemistry, Ministry of Agriculture, Nanjing Agriculture University, Nanjing, 210095, People's Republic of China. Electronic address: zhangyuanshu@njau.edu.cn.

Pub Type(s)

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

Language

eng

PubMed ID

25882007

Citation

Zhang, Wei, et al. "Beta-casomorphin-7 Prevents Epithelial-mesenchymal Transdifferentiation of NRK-52E Cells at High Glucose Level: Involvement of AngII-TGF-β1 Pathway." Peptides, vol. 70, 2015, pp. 37-44.
Zhang W, Song S, Liu F, et al. Beta-casomorphin-7 prevents epithelial-mesenchymal transdifferentiation of NRK-52E cells at high glucose level: Involvement of AngII-TGF-β1 pathway. Peptides. 2015;70:37-44.
Zhang, W., Song, S., Liu, F., Liu, Y., & Zhang, Y. (2015). Beta-casomorphin-7 prevents epithelial-mesenchymal transdifferentiation of NRK-52E cells at high glucose level: Involvement of AngII-TGF-β1 pathway. Peptides, 70, 37-44. https://doi.org/10.1016/j.peptides.2015.04.002
Zhang W, et al. Beta-casomorphin-7 Prevents Epithelial-mesenchymal Transdifferentiation of NRK-52E Cells at High Glucose Level: Involvement of AngII-TGF-β1 Pathway. Peptides. 2015;70:37-44. PubMed PMID: 25882007.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Beta-casomorphin-7 prevents epithelial-mesenchymal transdifferentiation of NRK-52E cells at high glucose level: Involvement of AngII-TGF-β1 pathway. AU - Zhang,Wei, AU - Song,Shangxin, AU - Liu,Fei, AU - Liu,Yi, AU - Zhang,Yuanshu, Y1 - 2015/04/14/ PY - 2015/02/24/received PY - 2015/04/01/revised PY - 2015/04/02/accepted PY - 2015/4/18/entrez PY - 2015/4/18/pubmed PY - 2016/3/24/medline KW - Angiotensin II KW - Diabetic nephropathy KW - Epithelial-mesenchymal transdifferentiation KW - NRK-52E KW - TGF-β1 KW - β-casomorphin-7 SP - 37 EP - 44 JF - Peptides JO - Peptides VL - 70 N2 - BACKGROUND: Hyperglycemia is the most important risk factor in the progression of renal fibrosis in diabetic kidney. Based on previous studies, β-casomorphin-7 may exert anti-fibrotic activities in diabetic rats. However, the role of β-casomorphin-7 in the pathogenesis of renal tubulointerstitial fibrosis remains unclear. Thus, this study was designed to investigate the protective effect of β-casomorphin-7 on epithelial-mesenchymal transition (EMT) of NRK-52E cells treated under hyperglycemic condition and to explore the possible mechanism. RESEARCH DESIGN AND METHODS: NRK-52E cells were cultured in high glucose (30 mM) for 3 days. Different concentrations of β-casomorphin-7, naloxone (antagonist of opioid receptor) and losartan (antagonist of angiotensin II type I receptor) were added in the culture. Expression of α-smooth muscle actin (α-SMA), E-cadherin, vimentin and cytokeratin19 mRNA were determined by real-time PCR. Protein levels of E-cadherin and α-SMA were analyzed by Western blotting. The concentrations of angiotensin (Ang) II and transforming growth factor β1 (TGF-β1) in the culture medium were determined. RESULTS: High glucose-induced up-regulation of vimentin mRNA and α-SMA mRNA and protein were significantly inhibited by β-casomorphin-7. On the contrary, high glucose-induced down-regulation of cytokeratin19 mRNA and E-cad mRNA and protein was significantly reversed by β-casomorphin-7. β-casomorphin-7 significantly alleviate high glucose induced increase of AngII and TGF-β1 in the culture. Moreover, losartan significantly attenuated the expression of TGF-β1 and EMT of NRK-52E cells treated under hyperglycemic condition. But naloxone did not affect the EMT of NRK-52E cells treated by high glucose and β-casomorphin-7. CONCLUSION: We demonstrate that β-casomorphin-7 has the potential to inhibit high glucose-induced renal proximal tubular EMT partly by modulating AngII-TGF-β1 pathway, but not by opioid receptor. SN - 1873-5169 UR - https://www.unboundmedicine.com/medline/citation/25882007/Beta_casomorphin_7_prevents_epithelial_mesenchymal_transdifferentiation_of_NRK_52E_cells_at_high_glucose_level:_Involvement_of_AngII_TGF_β1_pathway_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0196-9781(15)00107-2 DB - PRIME DP - Unbound Medicine ER -