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10.1172/jci.insight.92801 http://scihub22266oqcxt.onion/10.1172/jci.insight.92801 C5499362!5499362 !28679951     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28679951 &cmd=llinks): Failed to open stream: HTTP request failed! 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A salt-sensing kinase in T lymphocytes, SGK1, drives hypertension and hypertensive end-organ damage |pdf=|usr=}}{{28679951 }} gab.com Text A salt-sensing kinase in T lymphocytes, SGK1, drives hypertension and hypertensive end-organ damage JO: JCI Insight http://www.kidney.de/pget.php?&tw=1&pmid=28679951 #FOAvip We previously showed that angiotensin II (Ang II) increases T cell production of IL-17A, and that mice deficient in IL-17A have blunted hypertension and attenuated renal and vascular dysfunction. It was recently shown that salt enhances IL-17A production from CD4+ T cells via a serum- and glucocorticoid-regulated kinase 1-dependent (SGK1-dependent) pathway. Thus, we tested the hypothesis that SGK1 signaling in T cells promotes hypertension and contributes to end-organ damage. We show that loss of T cell SGK1 results in a blunted hypertensive response to Ang II infusion by 25 mmHg. Importantly, renal and vascular inflammation is abrogated in these mice compared with control mice. Furthermore, mice lacking T cell SGK1 are protected from Ang II-induced endothelial dysfunction and renal injury. Loss of T cell SGK1 also blunts blood pressure and vascular inflammation in response to deoxycorticosterone acetate-salt (DOCA-salt) hypertension. Finally, we demonstrate that the Na+-K+-2Cl- cotransporter 1 (NKCC1) is upregulated in Th17 cells and is necessary for the salt-induced increase in SGK1 and the IL-23 receptor. These studies demonstrate that T cell SGK1 and NKCC1 may be novel therapeutic targets for the treatment of hypertension and identify a potentially new mechanism by which salt contributes to hypertension. Twit Text FOAVip A salt-sensing kinase in T lymphocytes, SGK1, drives hypertension and hypertensive end-organ damage ????JCI Insight http://www.kidney.de/pget.php?&tw=1&pmid=28679951 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28679951 #FOAvip English Wikipedia <ref>{{Cite pmid|28679951 }}</ref> A salt-sensing kinase in T lymphocytes, SGK1, drives hypertension and hypertensive end-organ damage #MMPMID28679951 Norlander AE ; Saleh MA ; Pandey AK ; Itani HA ; Wu J ; Xiao L ; Kang J ; Dale BL ; Goleva SB ; Laroumanie F ; Du L ; Harrison DG ; Madhur MS JCI Insight 2017[Jul]; 2 (13 ): ä PMID28679951 show ga We previously showed that angiotensin II (Ang II) increases T cell production of IL-17A, and that mice deficient in IL-17A have blunted hypertension and attenuated renal and vascular dysfunction. It was recently shown that salt enhances IL-17A production from CD4+ T cells via a serum- and glucocorticoid-regulated kinase 1-dependent (SGK1-dependent) pathway. Thus, we tested the hypothesis that SGK1 signaling in T cells promotes hypertension and contributes to end-organ damage. We show that loss of T cell SGK1 results in a blunted hypertensive response to Ang II infusion by 25 mmHg. Importantly, renal and vascular inflammation is abrogated in these mice compared with control mice. Furthermore, mice lacking T cell SGK1 are protected from Ang II-induced endothelial dysfunction and renal injury. Loss of T cell SGK1 also blunts blood pressure and vascular inflammation in response to deoxycorticosterone acetate-salt (DOCA-salt) hypertension. Finally, we demonstrate that the Na+-K+-2Cl- cotransporter 1 (NKCC1) is upregulated in Th17 cells and is necessary for the salt-induced increase in SGK1 and the IL-23 receptor. These studies demonstrate that T cell SGK1 and NKCC1 may be novel therapeutic targets for the treatment of hypertension and identify a potentially new mechanism by which salt contributes to hypertension. äA salt-sensing kinase in T lymphocytes, SGK1, drives hypertension and (epmc).pdf DeepDyve Pubget Overpricing