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10.1016/j.isci.2018.09.014 http://scihub22266oqcxt.onion/10.1016/j.isci.2018.09.014 30293012!6174824!30293012     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=30293012&cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215       iScience 2018 ; 8 (?): 85-102 Nephropedia Template TP {{tp|p=30293012|t=2018. M1 Macrophage Polarization Is Dependent on TRPC1-Mediated Calcium Entry |pdf=|usr=}}{{30293012}} gab.com Text M1 Macrophage Polarization Is Dependent on TRPC1-Mediated Calcium Entry JO: iScience http://www.kidney.de/pget.php?&tw=1&pmid=30293012 #FOAvip Macrophage plasticity is essential for innate immunity, but in-depth signaling mechanism(s) regulating their functional phenotypes are ill-defined. Here we report that interferon (IFN) gamma priming of naive macrophages induces store-mediated Ca(2+) entry and inhibition of Ca(2+) entry impairs polarization to M1 inflammatory phenotype. In vitro and in vivo functional analyses revealed ORAI1 to be a primary contributor to basal Ca(2+) influx in macrophages, whereas IFNgamma-induced Ca(2+) influx was mediated by TRPC1. Deficiency of TRPC1 displayed abrogated IFNgamma-induced M1 inflammatory mediators in macrophages. In a preclinical model of peritonitis by Klebsiella pneumoniae infection, macrophages showed increased Ca(2+) influx, which was TRPC1 dependent. Macrophages from infected TRPC1(-/-) mice showed inhibited expression of M1-associated signature molecules. Furthermore, in human patients with systemic inflammatory response syndrome, the level of TRPC1 expression in circulating macrophages directly correlated with M1 inflammatory mediators. Overall, TRPC1-mediated Ca(2+) influx is essential for the induction/shaping of macrophage polarization to M1 inflammatory phenotype. Twit Text FOAVip M1 Macrophage Polarization Is Dependent on TRPC1-Mediated Calcium Entry ????iScience http://www.kidney.de/pget.php?&tw=1&pmid=30293012 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=30293012 #FOAvip English Wikipedia <ref>{{Cite pmid|30293012}}</ref> M1 Macrophage Polarization Is Dependent on TRPC1-Mediated Calcium Entry #MMPMID30293012 Chauhan A; Sun Y; Sukumaran P; Quenum Zangbede FO; Jondle CN; Sharma A; Evans DL; Chauhan P; Szlabick RE; Aaland MO; Birnbaumer L; Sharma J; Singh BB; Mishra BB iScience 2018[Oct]; 8 (?): 85-102 PMID30293012show ga Macrophage plasticity is essential for innate immunity, but in-depth signaling mechanism(s) regulating their functional phenotypes are ill-defined. Here we report that interferon (IFN) gamma priming of naive macrophages induces store-mediated Ca(2+) entry and inhibition of Ca(2+) entry impairs polarization to M1 inflammatory phenotype. In vitro and in vivo functional analyses revealed ORAI1 to be a primary contributor to basal Ca(2+) influx in macrophages, whereas IFNgamma-induced Ca(2+) influx was mediated by TRPC1. Deficiency of TRPC1 displayed abrogated IFNgamma-induced M1 inflammatory mediators in macrophages. In a preclinical model of peritonitis by Klebsiella pneumoniae infection, macrophages showed increased Ca(2+) influx, which was TRPC1 dependent. Macrophages from infected TRPC1(-/-) mice showed inhibited expression of M1-associated signature molecules. Furthermore, in human patients with systemic inflammatory response syndrome, the level of TRPC1 expression in circulating macrophages directly correlated with M1 inflammatory mediators. Overall, TRPC1-mediated Ca(2+) influx is essential for the induction/shaping of macrophage polarization to M1 inflammatory phenotype. ?M1 Macrophage Polarization Is Dependent on TRPC1-Mediated Calcium Entr(epmc).pdf DeepDyve Pubget Overpricing