Roles of I in the downregulation of eNOS Ser1177 phosphorylation by angiotensin II-activated PP2A.

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ID: 18798
2019
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Ranked #37 of 66 articles by views in Biochemical and biophysical research communications

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Abstract
The chronic elevation of angiotensin II (Ang II) is an important cause of endothelial dysfunction (ED). The Ang II/type 1 receptor (ATR) signaling pathway can cause endothelial nitric oxide synthase (eNOS)/nitric oxide (NO) dysfunction through various mechanisms leading to ED. The modulation of eNOS phosphorylated at Ser1177 is an important mechanism upregulating eNOS activity. Protein phosphatase 2 A (PP2A) has been reported to dephosphorylate eNOS at Ser1177. The PP2A inhibitor 2 protein (I) is a specific endogenous inhibitor that binds the catalytic subunit of PP2A and directly inhibits PP2A activity. Therefore, we hypothesized that Ang II might attenuate I expression to activate PP2A, which downregulates eNOS Ser 1177 phosphorylation, leading to eNOS dysfunction. In our study, we used Ang II-treated human umbilical vein endothelial cells (HUVECs) and, found that the eNOS Ser1177 phosphorylation levels were downregulated, the activity of PP2A was increased, and I expression was decreased. Furthermore, these effects were blocked by candesartan (CAN). The phosphorylation levels of eNOS Ser1177 were decreased after I was knocked down by specific siRNA but increased after I overexpression. We also found that the Ang II treatment decreased the association of I with PP2A but increased the association between PP2A and eNOS. Taken together, our results suggest that Ang II activates PP2A by downregulating the I expression through the ATR signaling pathway leading to the loss of eNOS Ser1177 phosphorylation and ED.
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luo2019rolesbiochemical Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
Authors Luo, Yanbei;Zhang, Qian;Ding, Jing;Yu, Min;Jiang, Juncai;Yang, Fei;Wang, Shengnan;Wang, Alei;Wang, Lingxiao;Wu, Shan;Xia, Yong;Lu, Deqin;
Journal Biochemical and biophysical research communications
Year 2019
DOI
S0006-291X(19)31199-4
URL
Keywords Keywords not found

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