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10.1111/jth.13578 http://scihub22266oqcxt.onion/10.1111/jth.13578 C5396324!5396324 !27896950     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27896950 &cmd=llinks): Failed to open stream: HTTP request failed! 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PPAR? agonists negatively regulate ?IIb?3 integrin outside-in signaling and platelet function through up-regulation of protein kinase A activity |pdf=|usr=}}{{27896950 }} gab.com Text PPAR agonists negatively regulate IIb 3 integrin outside-in signaling and platelet function through up-regulation of protein kinase A activity JO: J Thromb Haemost http://www.kidney.de/pget.php?&tw=1&pmid=27896950 #FOAvip Essentials peroxisome proliferator-activated receptor ? (PPAR?) agonists inhibit platelet function. PPAR? agonists negatively regulate outside-in signaling via integrin ?IIb?3. PPAR? agonists disrupt the interaction of G?13 with integrin ?3. This is attributed to an upregulation of protein kinase A activity. SUMMARY: Background Agonists for the peroxisome proliferator-activated receptor (PPAR?) have been shown to have inhibitory effects on platelet activity following stimulation by GPVI and GPCR agonists. Objectives Profound effects on thrombus formation led us to suspect a role for PPAR? agonists in the regulation of integrin ?IIb?3 mediated signaling. Both GPVI and GPCR signaling pathways lead to ?IIb?3 activation, and signaling through ?IIb?3 plays a critical role in platelet function and normal hemostasis. Methods The effects of PPAR? agonists on the regulation of ?IIb?3 outside-in signaling was determined by monitoring the ability of platelets to adhere and spread on fibrinogen and undergo clot retraction. Effects on signaling components downstream of ?IIb?3 activation were also determined following adhesion to fibrinogen by Western blotting. Results Treatment of platelets with PPAR? agonists inhibited platelet adhesion and spreading on fibrinogen and diminished clot retraction. A reduction in phosphorylation of several components of ?IIb?3 signaling, including the integrin ?3 subunit, Syk, PLC?2, focal adhesion kinase (FAK) and Akt, was also observed as a result of reduced interaction of the integrin ?3 subunit with G?13. Studies of VASP phosphorylation revealed that this was because of an increase in PKA activity following treatment with PPAR? receptor agonists. Conclusions This study provides further evidence for antiplatelet actions of PPAR? agonists, identifies a negative regulatory role for PPAR? agonists in the control of integrin ?IIb?3 outside-in signaling, and provides a molecular basis by which the PPAR? agonists negatively regulate platelet activation and thrombus formation. Twit Text FOAVip PPAR agonists negatively regulate IIb 3 integrin outside-in signaling and platelet function through up-regulation of protein kinase A activity ????J Thromb Haemost http://www.kidney.de/pget.php?&tw=1&pmid=27896950 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27896950 #FOAvip English Wikipedia <ref>{{Cite pmid|27896950 }}</ref> PPAR? agonists negatively regulate ?IIb?3 integrin outside-in signaling and platelet function through up-regulation of protein kinase A activity #MMPMID27896950 Unsworth AJ ; Kriek N ; Bye AP ; Naran K ; Sage T ; Flora GD ; Gibbins JM J Thromb Haemost 2017[Feb]; 15 (2 ): 356-369 PMID27896950 show ga Essentials peroxisome proliferator-activated receptor ? (PPAR?) agonists inhibit platelet function. PPAR? agonists negatively regulate outside-in signaling via integrin ?IIb?3. PPAR? agonists disrupt the interaction of G?13 with integrin ?3. This is attributed to an upregulation of protein kinase A activity. SUMMARY: Background Agonists for the peroxisome proliferator-activated receptor (PPAR?) have been shown to have inhibitory effects on platelet activity following stimulation by GPVI and GPCR agonists. Objectives Profound effects on thrombus formation led us to suspect a role for PPAR? agonists in the regulation of integrin ?IIb?3 mediated signaling. Both GPVI and GPCR signaling pathways lead to ?IIb?3 activation, and signaling through ?IIb?3 plays a critical role in platelet function and normal hemostasis. Methods The effects of PPAR? agonists on the regulation of ?IIb?3 outside-in signaling was determined by monitoring the ability of platelets to adhere and spread on fibrinogen and undergo clot retraction. Effects on signaling components downstream of ?IIb?3 activation were also determined following adhesion to fibrinogen by Western blotting. Results Treatment of platelets with PPAR? agonists inhibited platelet adhesion and spreading on fibrinogen and diminished clot retraction. A reduction in phosphorylation of several components of ?IIb?3 signaling, including the integrin ?3 subunit, Syk, PLC?2, focal adhesion kinase (FAK) and Akt, was also observed as a result of reduced interaction of the integrin ?3 subunit with G?13. Studies of VASP phosphorylation revealed that this was because of an increase in PKA activity following treatment with PPAR? receptor agonists. Conclusions This study provides further evidence for antiplatelet actions of PPAR? agonists, identifies a negative regulatory role for PPAR? agonists in the control of integrin ?IIb?3 outside-in signaling, and provides a molecular basis by which the PPAR? agonists negatively regulate platelet activation and thrombus formation. |Animals [MESH] |Blood Platelets/*metabolism [MESH] |Cattle [MESH] |Cell Adhesion [MESH] |Clot Retraction [MESH] |Collagen/chemistry [MESH] |Cyclic AMP-Dependent Protein Kinases/*metabolism [MESH] |Fibrinogen/chemistry [MESH] |GTP-Binding Protein alpha Subunits, G12-G13/metabolism [MESH] |Hemostasis [MESH] |Humans [MESH] |Integrin beta3/metabolism [MESH] |PPAR gamma/*agonists [MESH] |Phosphorylation [MESH] |Platelet Activation/drug effects [MESH] |Platelet Adhesiveness [MESH] |Platelet Aggregation/drug effects [MESH] |Platelet Function Tests [MESH] |Platelet Glycoprotein GPIIb-IIIa Complex/*metabolism [MESH] |Platelet Membrane Glycoproteins/metabolism [MESH] |Signal Transduction [MESH]PPAR? agonists negatively regulate ?IIb?3 integrin outside-in signalin(epmc).pdf DeepDyve Pubget Overpricing