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10.1210/me.2014-1388 http://scihub22266oqcxt.onion/10.1210/me.2014-1388 C4447644!4447644 !25871850     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=25871850 &cmd=llinks): Failed to open stream: HTTP request failed! 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Inhibition of Sphingosine Kinase 1 Ameliorates Angiotensin II-Induced Hypertension and Inhibits Transmembrane Calcium Entry via Store-Operated Calcium Channel |pdf=|usr=}}{{25871850 }} gab.com Text Inhibition of Sphingosine Kinase 1 Ameliorates Angiotensin II-Induced Hypertension and Inhibits Transmembrane Calcium Entry via Store-Operated Calcium Channel JO: Mol Endocrinol http://www.kidney.de/pget.php?&tw=1&pmid=25871850 #FOAvip Angiotensin II (AngII) plays a critical role in the regulation of vascular tone and blood pressure mainly via regulation of Ca(2+) mobilization. Several reports have implicated sphingosine kinase 1 (SK1)/sphingosine 1-phosphate (S1P) in the mobilization of intracellular Ca(2+) through a yet-undefined mechanism. Here we demonstrate that AngII-induces biphasic calcium entry in vascular smooth muscle cells, consisting of an immediate peak due to inositol tris-phosphate-dependent release of intracellular calcium, followed by a sustained transmembrane Ca(2+) influx through store-operated calcium channels (SOCs). Inhibition of SK1 attenuates the second phase of transmembrane Ca(2+) influx, suggesting a role for SK1 in AngII-dependent activation of SOC. Intracellular S1P triggers SOC-dependent Ca(2+) influx independent of S1P receptors, whereas external application of S1P stimulated S1P receptor-dependent Ca(2+) influx that is insensitive to inhibitors of SOCs, suggesting that the SK1/S1P axis regulates store-operated calcium entry via intracellular rather than extracellular actions. Genetic deletion of SK1 significantly inhibits both the acute hypertensive response to AngII in anaesthetized SK1 knockout mice and the sustained hypertensive response to continuous infusion of AngII in conscious animals. Collectively these data implicate SK1 as the missing link that connects the angiotensin AT1A receptor to transmembrane Ca(2+) influx and identify SOCs as a potential intracellular target for SK1. Twit Text FOAVip Inhibition of Sphingosine Kinase 1 Ameliorates Angiotensin II-Induced Hypertension and Inhibits Transmembrane Calcium Entry via Store-Operated Calcium Channel ????Mol Endocrinol http://www.kidney.de/pget.php?&tw=1&pmid=25871850 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25871850 #FOAvip English Wikipedia <ref>{{Cite pmid|25871850 }}</ref> Inhibition of Sphingosine Kinase 1 Ameliorates Angiotensin II-Induced Hypertension and Inhibits Transmembrane Calcium Entry via Store-Operated Calcium Channel #MMPMID25871850 Wilson PC ; Fitzgibbon WR ; Garrett SM ; Jaffa AA ; Luttrell LM ; Brands MW ; El-Shewy HM Mol Endocrinol 2015[Jun]; 29 (6 ): 896-908 PMID25871850 show ga Angiotensin II (AngII) plays a critical role in the regulation of vascular tone and blood pressure mainly via regulation of Ca(2+) mobilization. Several reports have implicated sphingosine kinase 1 (SK1)/sphingosine 1-phosphate (S1P) in the mobilization of intracellular Ca(2+) through a yet-undefined mechanism. Here we demonstrate that AngII-induces biphasic calcium entry in vascular smooth muscle cells, consisting of an immediate peak due to inositol tris-phosphate-dependent release of intracellular calcium, followed by a sustained transmembrane Ca(2+) influx through store-operated calcium channels (SOCs). Inhibition of SK1 attenuates the second phase of transmembrane Ca(2+) influx, suggesting a role for SK1 in AngII-dependent activation of SOC. Intracellular S1P triggers SOC-dependent Ca(2+) influx independent of S1P receptors, whereas external application of S1P stimulated S1P receptor-dependent Ca(2+) influx that is insensitive to inhibitors of SOCs, suggesting that the SK1/S1P axis regulates store-operated calcium entry via intracellular rather than extracellular actions. Genetic deletion of SK1 significantly inhibits both the acute hypertensive response to AngII in anaesthetized SK1 knockout mice and the sustained hypertensive response to continuous infusion of AngII in conscious animals. Collectively these data implicate SK1 as the missing link that connects the angiotensin AT1A receptor to transmembrane Ca(2+) influx and identify SOCs as a potential intracellular target for SK1. |Angiotensin II [MESH] |Animals [MESH] |Blood Pressure/drug effects [MESH] |Calcium Channels/*metabolism [MESH] |Calcium/*metabolism [MESH] |Cell Membrane/drug effects/metabolism [MESH] |Chronic Disease [MESH] |Enzyme Activation/drug effects [MESH] |Gene Deletion [MESH] |HEK293 Cells [MESH] |Humans [MESH] |Hypertension/*enzymology/*pathology/physiopathology [MESH] |Lysophospholipids/biosynthesis/pharmacology [MESH] |Male [MESH] |Mice, Inbred C57BL [MESH] |Phosphotransferases (Alcohol Group Acceptor)/*antagonists & inhibitors/metabolism [MESH] |Rats, Sprague-Dawley [MESH] |Receptors, Lysosphingolipid/metabolism [MESH]Inhibition of Sphingosine Kinase 1 Ameliorates Angiotensin II-Induced (epmc).pdf DeepDyve Pubget Overpricing