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10.1016/j.atherosclerosis.2017.02.021 http://scihub22266oqcxt.onion/10.1016/j.atherosclerosis.2017.02.021 C5395299!5395299!28286252     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Atherosclerosis 2017 ; 259 (ä): 51-9 Nephropedia Template TP {{tp|p=28286252|t=2017. PKC-epsilon and TLR4 synergistically regulate resistin-mediated inflammation in human macrophages |pdf=|usr=}}{{28286252}} gab.com Text PKC-epsilon and TLR4 synergistically regulate resistin-mediated inflammation in human macrophages JO: Atherosclerosis http://www.kidney.de/pget.php?&tw=1&pmid=28286252 #FOAvip Background and aims: Resistin has been associated with atherosclerotic inflammation and cardiovascular complications. We and others have previously shown that PKC-epsilon (PKC?) is involved in resistin-induced smooth muscle cell (VSMC) dysfunction at a high pathological concentration. This study aimed to evaluate the role and potential pathways of resistin at a physiological concentration, in atherosclerosis-related inflammation. Methods: Plasma from patients with atherosclerosis was analyzed for resistin concentration. Patients were divided into tertiles based on resistin levels and cytokines were compared between tertiles. Macrophages were then treated with resistin in the presence or absence of PKC? inhibitor and/or TLR4 blocking-antibody, and their inflammatory state was evaluated with ELISA, RT-PCR, immunocytochemistry, and Western blot. Results: We observed significant associations between plasma resistin levels and TNF-?, IL-6, IL-12, MIP-1?, MIP-1?, and CD40L. Our in vitro analyses revealed that resistin activated PKC? via TLR4. This was followed by NF-kB activation and induction of a pro-inflammatory phenotype in macrophages, significantly upregulating CD40, downregulating CD206 and stimulating gene expression and secretion of the inflammatory cytokines, for which we found association in our plasma analysis. Resistin also induced persistent TRAM and CD40L upregulation up to 36 hours after resistin treatment. PKC? and TLR4 inhibitors suppressed gene expression to levels similar to control, especially when used in combination. Conclusions: Resistin, at a physiological concentration, exacerbates the inflammatory response of macrophages. PKC? is a key upstream mediator in resistin-induced inflammation that may interact synergistically with TLR4 to promote NF-kB activation, while TRAM is an important signal. PKC? and TRAM may represent novel molecular targets for resistin-associated chronic atherosclerotic inflammation. Twit Text FOAVip PKC-epsilon and TLR4 synergistically regulate resistin-mediated inflammation in human macrophages ????Atherosclerosis http://www.kidney.de/pget.php?&tw=1&pmid=28286252 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28286252 #FOAvip English Wikipedia <ref>{{Cite pmid|28286252}}</ref> PKC-epsilon and TLR4 synergistically regulate resistin-mediated inflammation in human macrophages #MMPMID28286252 Zuniga MC; Raghuraman G; Hitchner E; Weyand C; Robinson W; Zhou W Atherosclerosis 2017[Apr]; 259 (ä): 51-9 PMID28286252show ga Background and aims: Resistin has been associated with atherosclerotic inflammation and cardiovascular complications. We and others have previously shown that PKC-epsilon (PKC?) is involved in resistin-induced smooth muscle cell (VSMC) dysfunction at a high pathological concentration. This study aimed to evaluate the role and potential pathways of resistin at a physiological concentration, in atherosclerosis-related inflammation. Methods: Plasma from patients with atherosclerosis was analyzed for resistin concentration. Patients were divided into tertiles based on resistin levels and cytokines were compared between tertiles. Macrophages were then treated with resistin in the presence or absence of PKC? inhibitor and/or TLR4 blocking-antibody, and their inflammatory state was evaluated with ELISA, RT-PCR, immunocytochemistry, and Western blot. Results: We observed significant associations between plasma resistin levels and TNF-?, IL-6, IL-12, MIP-1?, MIP-1?, and CD40L. Our in vitro analyses revealed that resistin activated PKC? via TLR4. This was followed by NF-kB activation and induction of a pro-inflammatory phenotype in macrophages, significantly upregulating CD40, downregulating CD206 and stimulating gene expression and secretion of the inflammatory cytokines, for which we found association in our plasma analysis. Resistin also induced persistent TRAM and CD40L upregulation up to 36 hours after resistin treatment. PKC? and TLR4 inhibitors suppressed gene expression to levels similar to control, especially when used in combination. Conclusions: Resistin, at a physiological concentration, exacerbates the inflammatory response of macrophages. PKC? is a key upstream mediator in resistin-induced inflammation that may interact synergistically with TLR4 to promote NF-kB activation, while TRAM is an important signal. PKC? and TRAM may represent novel molecular targets for resistin-associated chronic atherosclerotic inflammation. äPKC-epsilon and TLR4 synergistically regulate resistin-mediated inflam(epmc).pdf DeepDyve Pubget Overpricing