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10.1161/CIRCULATIONAHA.112.132126 http://scihub22266oqcxt.onion/10.1161/CIRCULATIONAHA.112.132126 C4472638!4472638 !23266857     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=23266857 &cmd=llinks): Failed to open stream: HTTP request failed! 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Signal transducer and activator of transcription 3 (STAT3) regulates collagen-induced platelet aggregation independently of its transcription factor activity |pdf=|usr=}}{{23266857 }} gab.com Text Signal transducer and activator of transcription 3 (STAT3) regulates collagen-induced platelet aggregation independently of its transcription factor activity JO: Circulation http://www.kidney.de/pget.php?&tw=1&pmid=23266857 #FOAvip BACKGROUND: Platelet hyperactivity induced by inflammation is a known risk factor for atherosclerosis and thrombosis, but its underlying mechanisms remain poorly understood. METHODS AND RESULTS: The signal transducer and activator of transcription 3 (STAT3) was activated in collagen-stimulated platelets. Activated STAT3 served as a protein scaffold to facilitate the catalytic interaction between the kinase Syk (spleen tyrosine kinase) and the substrate PLC?2 to enhance collagen-induced calcium mobilization and platelet activation. The same interaction of STAT3 with Syk and PLC?2 was detected in HEK293 cells transfected with cDNAs for Syk and PLC?2 and stimulated with interleukin-6. Pharmacological inhibition of STAT3 blocked ?50% of collagen- and a collagen-related peptide-induced but not thrombin receptor-activating peptide- or ADP-induced aggregation and ?80% of thrombus formation of human platelets on a collagen matrix. This in vitro phenotype was reproduced in mice infused with STAT3 inhibitors and mice with platelet-specific STAT3 deficiency. By forming a complex with its soluble receptor, the proinflammatory cytokine interleukin-6 enhanced the collagen-induced STAT3 activation in human platelets. CONCLUSIONS: These data demonstrate a nontranscriptional activity of STAT3 that facilitates a crosstalk between proinflammatory cytokine and hemostasis/thrombosis signals in platelets. This crosstalk may be responsible for the platelet hyperactivity found in conditions of inflammation. Twit Text FOAVip Signal transducer and activator of transcription 3 (STAT3) regulates collagen-induced platelet aggregation independently of its transcription factor activity ????Circulation http://www.kidney.de/pget.php?&tw=1&pmid=23266857 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=23266857 #FOAvip English Wikipedia <ref>{{Cite pmid|23266857 }}</ref> Signal transducer and activator of transcription 3 (STAT3) regulates collagen-induced platelet aggregation independently of its transcription factor activity #MMPMID23266857 Zhou Z ; Gushiken FC ; Bolgiano D ; Salsbery BJ ; Aghakasiri N ; Jing N ; Wu X ; Vijayan KV ; Rumbaut RE ; Adachi R ; Lopez JA ; Dong JF Circulation 2013[Jan]; 127 (4 ): 476-485 PMID23266857 show ga BACKGROUND: Platelet hyperactivity induced by inflammation is a known risk factor for atherosclerosis and thrombosis, but its underlying mechanisms remain poorly understood. METHODS AND RESULTS: The signal transducer and activator of transcription 3 (STAT3) was activated in collagen-stimulated platelets. Activated STAT3 served as a protein scaffold to facilitate the catalytic interaction between the kinase Syk (spleen tyrosine kinase) and the substrate PLC?2 to enhance collagen-induced calcium mobilization and platelet activation. The same interaction of STAT3 with Syk and PLC?2 was detected in HEK293 cells transfected with cDNAs for Syk and PLC?2 and stimulated with interleukin-6. Pharmacological inhibition of STAT3 blocked ?50% of collagen- and a collagen-related peptide-induced but not thrombin receptor-activating peptide- or ADP-induced aggregation and ?80% of thrombus formation of human platelets on a collagen matrix. This in vitro phenotype was reproduced in mice infused with STAT3 inhibitors and mice with platelet-specific STAT3 deficiency. By forming a complex with its soluble receptor, the proinflammatory cytokine interleukin-6 enhanced the collagen-induced STAT3 activation in human platelets. CONCLUSIONS: These data demonstrate a nontranscriptional activity of STAT3 that facilitates a crosstalk between proinflammatory cytokine and hemostasis/thrombosis signals in platelets. This crosstalk may be responsible for the platelet hyperactivity found in conditions of inflammation. |Animals [MESH] |Atherosclerosis/metabolism [MESH] |Blood Platelets/cytology/drug effects/metabolism [MESH] |Collagen/metabolism/pharmacology [MESH] |HEK293 Cells [MESH] |Humans [MESH] |Interleukin-6/metabolism [MESH] |Intracellular Signaling Peptides and Proteins/antagonists & inhibitors/metabolism [MESH] |Mice [MESH] |Mice, Inbred C57BL [MESH] |Mice, Knockout [MESH] |Phospholipase C gamma/metabolism [MESH] |Phosphorylation/physiology [MESH] |Platelet Aggregation/*physiology [MESH] |Protein-Tyrosine Kinases/antagonists & inhibitors/metabolism [MESH] |STAT3 Transcription Factor/genetics/*metabolism [MESH] |Signal Transduction/*physiology [MESH] |Syk Kinase [MESH] |Thrombosis/metabolism [MESH]Signal transducer and activator of transcription 3 (STAT3) regulates (epmc).pdf DeepDyve Pubget Overpricing