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Angiotensin-(1-7) attenuates high glucose-induced proximal tubular epithelial-to-mesenchymal transition via inhibiting ERK1/2 and p38 phosphorylation.
Life Sci. 2012 Mar 10; 90(11-12):454-62.LS

Abstract

AIMS

The kidney is an important target for both Angiotensin II and angiotensin-(1-7) [Ang-(1-7)] in the renin-angiotensin system. However, the renal function of Ang-(1-7) remains unclear. This study is aimed at investigating the effect of Ang-(1-7) on high glucose-induced epithelial to mesenchymal transition (EMT) in cultured renal epithelial cells.

MAIN METHODS

Cultured renal epithelial (NRK-52E) cell line was used in the experiment. Fluorescence immunocytochemistry was performed to observe α-smooth muscle actin (α-SMA). Real-time PCR and Western blot were used to determine mRNA and protein levels. Enzyme-linked immunosorbent assay was used to measure the concentration of transforming growth factor-β1 (TGF-β1) in the culture media.

KEY FINDINGS

High glucose-induced decreased in both angiotensin-converting enzyme-related carboxypeptidase (ACE2) and Mas mRNA levels. Meanwhile, high glucose induced increases in α-SMA and vimentin, decreases in E-cadherin, elevations in TGF-β1 and fibronectin secretions. Ang-(1-7) partially reversed high glucose-induced changes in α-SMA, vimentin, E-cadherin, TGF-β1 and fibronectin. High glucose stimulated ERK, p38 and JNK phosphorylation and Ang-(1-7) reversed the changes in ERK and p38 but not JNK phosphorylation.

SIGNIFICANCE

Inhibition and insufficiency in ACE2-Ang-(1-7)-Mas axis under high glucose condition participate EMT. Supplementation of Ang-(1-7) attenuates high glucose-induced EMT. ERK and p38 intracellular signaling pathways, not JNK, mediate the effect of Ang-(1-7) on EMT.

Authors+Show Affiliations

Department of Physiology and Pathophysiology, Shanghai Medical College, Fudan University Shanghai 200032, China.No 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

22285598

Citation

Zhou, Li, et al. "Angiotensin-(1-7) Attenuates High Glucose-induced Proximal Tubular Epithelial-to-mesenchymal Transition Via Inhibiting ERK1/2 and P38 Phosphorylation." Life Sciences, vol. 90, no. 11-12, 2012, pp. 454-62.
Zhou L, Xue H, Wang Z, et al. Angiotensin-(1-7) attenuates high glucose-induced proximal tubular epithelial-to-mesenchymal transition via inhibiting ERK1/2 and p38 phosphorylation. Life Sci. 2012;90(11-12):454-62.
Zhou, L., Xue, H., Wang, Z., Ni, J., Yao, T., Huang, Y., Yu, C., & Lu, L. (2012). Angiotensin-(1-7) attenuates high glucose-induced proximal tubular epithelial-to-mesenchymal transition via inhibiting ERK1/2 and p38 phosphorylation. Life Sciences, 90(11-12), 454-62. https://doi.org/10.1016/j.lfs.2011.12.015
Zhou L, et al. Angiotensin-(1-7) Attenuates High Glucose-induced Proximal Tubular Epithelial-to-mesenchymal Transition Via Inhibiting ERK1/2 and P38 Phosphorylation. Life Sci. 2012 Mar 10;90(11-12):454-62. PubMed PMID: 22285598.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Angiotensin-(1-7) attenuates high glucose-induced proximal tubular epithelial-to-mesenchymal transition via inhibiting ERK1/2 and p38 phosphorylation. AU - Zhou,Li, AU - Xue,Hong, AU - Wang,Zhen, AU - Ni,Jun, AU - Yao,Tai, AU - Huang,Yu, AU - Yu,Chen, AU - Lu,Limin, Y1 - 2012/01/18/ PY - 2011/08/11/received PY - 2011/12/03/revised PY - 2011/12/29/accepted PY - 2012/1/31/entrez PY - 2012/1/31/pubmed PY - 2012/4/24/medline SP - 454 EP - 62 JF - Life sciences JO - Life Sci. VL - 90 IS - 11-12 N2 - AIMS: The kidney is an important target for both Angiotensin II and angiotensin-(1-7) [Ang-(1-7)] in the renin-angiotensin system. However, the renal function of Ang-(1-7) remains unclear. This study is aimed at investigating the effect of Ang-(1-7) on high glucose-induced epithelial to mesenchymal transition (EMT) in cultured renal epithelial cells. MAIN METHODS: Cultured renal epithelial (NRK-52E) cell line was used in the experiment. Fluorescence immunocytochemistry was performed to observe α-smooth muscle actin (α-SMA). Real-time PCR and Western blot were used to determine mRNA and protein levels. Enzyme-linked immunosorbent assay was used to measure the concentration of transforming growth factor-β1 (TGF-β1) in the culture media. KEY FINDINGS: High glucose-induced decreased in both angiotensin-converting enzyme-related carboxypeptidase (ACE2) and Mas mRNA levels. Meanwhile, high glucose induced increases in α-SMA and vimentin, decreases in E-cadherin, elevations in TGF-β1 and fibronectin secretions. Ang-(1-7) partially reversed high glucose-induced changes in α-SMA, vimentin, E-cadherin, TGF-β1 and fibronectin. High glucose stimulated ERK, p38 and JNK phosphorylation and Ang-(1-7) reversed the changes in ERK and p38 but not JNK phosphorylation. SIGNIFICANCE: Inhibition and insufficiency in ACE2-Ang-(1-7)-Mas axis under high glucose condition participate EMT. Supplementation of Ang-(1-7) attenuates high glucose-induced EMT. ERK and p38 intracellular signaling pathways, not JNK, mediate the effect of Ang-(1-7) on EMT. SN - 1879-0631 UR - https://www.unboundmedicine.com/medline/citation/22285598/Angiotensin__1_7__attenuates_high_glucose_induced_proximal_tubular_epithelial_to_mesenchymal_transition_via_inhibiting_ERK1/2_and_p38_phosphorylation_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0024-3205(12)00004-5 DB - PRIME DP - Unbound Medicine ER -