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10.1016/j.bbrc.2012.02.015 http://scihub22266oqcxt.onion/10.1016/j.bbrc.2012.02.015 22424098!ä!22424098 Deprecated: Implicit conversion from float 215.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 215.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 215.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 215.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 215.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 215.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 215.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 215.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 249.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Biochem+Biophys+Res+Commun 2012 ; 419 (3): 466-71 Nephropedia Template TP {{tp|p=22424098|t=2012. PI3K/Akt contributes to increased expression of Toll-like receptor 4 in macrophages exposed to hypoxic stress |pdf=|usr=}}{{22424098}} gab.com Text PI3K/Akt contributes to increased expression of Toll-like receptor 4 in macrophages exposed to hypoxic stress JO: Biochem Biophys Res Commun http://www.kidney.de/pget.php?&tw=1&pmid=22424098 #FOAvip Toll-like receptors (TLRs) play critical roles in triggering immune and inflammatory responses by detecting invading microbial pathogens and endogenous danger signals. Increased expression of TLR4 is implicated in aggravated inflammatory symptoms in ischemic tissue injury and chronic diseases. Results from our previous study showed that TLR4 expression was upregulated by hypoxic stress mediated by hypoxia-inducible factor-1 (HIF-1) at a transcriptional level in macrophages. In this study, we further investigated the upstream signaling pathway that contributed to the increase of TLR4 expression by hypoxic stress. Either treatment with pharmacological inhibitors of PI3K and Akt or knockdown of Akt expression by siRNA blocked the increase of TLR4 mRNA and protein levels in macrophages exposed to hypoxia and CoCl(2). Phosphorylation of Akt by hypoxic stress preceded nuclear accumulation of HIF-1alpha. A PI3K inhibitor (LY294002) attenuated CoCl(2)-induced nuclear accumulation and transcriptional activation of HIF-1alpha. In addition, HIF-1alpha-mediated upregulation of TLR4 expression was blocked by LY294002. Furthermore, sulforaphane suppressed hypoxia- and CoCl(2)-induced upregulation of TLR4 mRNA and protein by inhibiting PI3K/Akt activation and the subsequent nuclear accumulation and transcriptional activation of HIF-1alpha. However, p38 was not involved in HIF-1alpha activation and TLR4 expression induced by hypoxic stress in macrophages. Collectively, our results demonstrate that PI3K/Akt contributes to hypoxic stress-induced TLR4 expression at least partly through the regulation of HIF-1 activation. These reveal a novel mechanism for regulation of TLR4 expression upon hypoxic stress and provide a therapeutic target for chronic diseases related to hypoxic stress. Twit Text FOAVip PI3K/Akt contributes to increased expression of Toll-like receptor 4 in macrophages exposed to hypoxic stress ????Biochem Biophys Res Commun http://www.kidney.de/pget.php?&tw=1&pmid=22424098 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=22424098 #FOAvip English Wikipedia <ref>{{Cite pmid|22424098}}</ref> PI3K/Akt contributes to increased expression of Toll-like receptor 4 in macrophages exposed to hypoxic stress #MMPMID22424098 Kim SY; Jeong E; Joung SM; Lee JY Biochem Biophys Res Commun 2012[Mar]; 419 (3): 466-71 PMID22424098show ga Toll-like receptors (TLRs) play critical roles in triggering immune and inflammatory responses by detecting invading microbial pathogens and endogenous danger signals. Increased expression of TLR4 is implicated in aggravated inflammatory symptoms in ischemic tissue injury and chronic diseases. Results from our previous study showed that TLR4 expression was upregulated by hypoxic stress mediated by hypoxia-inducible factor-1 (HIF-1) at a transcriptional level in macrophages. In this study, we further investigated the upstream signaling pathway that contributed to the increase of TLR4 expression by hypoxic stress. Either treatment with pharmacological inhibitors of PI3K and Akt or knockdown of Akt expression by siRNA blocked the increase of TLR4 mRNA and protein levels in macrophages exposed to hypoxia and CoCl(2). Phosphorylation of Akt by hypoxic stress preceded nuclear accumulation of HIF-1alpha. A PI3K inhibitor (LY294002) attenuated CoCl(2)-induced nuclear accumulation and transcriptional activation of HIF-1alpha. In addition, HIF-1alpha-mediated upregulation of TLR4 expression was blocked by LY294002. Furthermore, sulforaphane suppressed hypoxia- and CoCl(2)-induced upregulation of TLR4 mRNA and protein by inhibiting PI3K/Akt activation and the subsequent nuclear accumulation and transcriptional activation of HIF-1alpha. However, p38 was not involved in HIF-1alpha activation and TLR4 expression induced by hypoxic stress in macrophages. Collectively, our results demonstrate that PI3K/Akt contributes to hypoxic stress-induced TLR4 expression at least partly through the regulation of HIF-1 activation. These reveal a novel mechanism for regulation of TLR4 expression upon hypoxic stress and provide a therapeutic target for chronic diseases related to hypoxic stress. |*Stress, Physiological[MESH] |Animals[MESH] |Cell Hypoxia[MESH] |Cell Line[MESH] |Chromones/pharmacology[MESH] |Cobalt/pharmacology[MESH] |Gene Knockdown Techniques[MESH] |Hypoxia-Inducible Factor 1, alpha Subunit/genetics/metabolism[MESH] |Isothiocyanates[MESH] |Macrophages/metabolism/physiology[MESH] |Mice[MESH] |Morpholines/pharmacology[MESH] |Phosphatidylinositol 3-Kinases/*metabolism[MESH] |Phosphoinositide-3 Kinase Inhibitors[MESH] |Phosphorylation[MESH] |Proto-Oncogene Proteins c-akt/antagonists & inhibitors/genetics/*metabolism[MESH] |RNA, Messenger/biosynthesis[MESH] |Sulfoxides[MESH] |Thiocyanates/pharmacology[MESH] |Toll-Like Receptor 4/*biosynthesis[MESH] |Transcription, Genetic[MESH]PI3K/Akt contributes to increased expression of Toll-like receptor 4 i(epmc).pdf DeepDyve Pubget Overpricing