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10.1172/jci.insight.151527 http://scihub22266oqcxt.onion/10.1172/jci.insight.151527 34506304!8564889!34506304     free     free     free Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       JCI+Insight 2021 ; 6 (20): ä Nephropedia Template TP {{tp|p=34506304|t=2021. Tie2 activation protects against prothrombotic endothelial dysfunction in COVID-19 |pdf=|usr=}}{{34506304}} gab.com Text Tie2 activation protects against prothrombotic endothelial dysfunction in COVID-19 JO: JCI Insight http://www.kidney.de/pget.php?&tw=1&pmid=34506304 #FOAvip Endothelial dysfunction accompanies the microvascular thrombosis commonly observed in severe COVID-19. Constitutively, the endothelial surface is anticoagulant, a property maintained at least in part via signaling through the Tie2 receptor. During inflammation, the Tie2 antagonist angiopoietin-2 (Angpt-2) is released from endothelial cells and inhibits Tie2, promoting a prothrombotic phenotypic shift. We sought to assess whether severe COVID-19 is associated with procoagulant endothelial dysfunction and alterations in the Tie2/angiopoietin axis. Primary HUVECs treated with plasma from patients with severe COVID-19 upregulated the expression of thromboinflammatory genes, inhibited the expression of antithrombotic genes, and promoted coagulation on the endothelial surface. Pharmacologic activation of Tie2 with the small molecule AKB-9778 reversed the prothrombotic state induced by COVID-19 plasma in primary endothelial cells. Lung autopsies from patients with COVID-19 demonstrated a prothrombotic endothelial signature. Assessment of circulating endothelial markers in a cohort of 98 patients with mild, moderate, or severe COVID-19 revealed endothelial dysfunction indicative of a prothrombotic state. Angpt-2 concentrations rose with increasing disease severity, and the highest levels were associated with worse survival. These data highlight the disruption of Tie2/angiopoietin signaling and procoagulant changes in endothelial cells in severe COVID-19. Our findings provide rationale for current trials of Tie2-activating therapy with AKB-9778 in COVID-19. Twit Text FOAVip Tie2 activation protects against prothrombotic endothelial dysfunction in COVID-19 ????JCI Insight http://www.kidney.de/pget.php?&tw=1&pmid=34506304 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=34506304 #FOAvip English Wikipedia <ref>{{Cite pmid|34506304}}</ref> Tie2 activation protects against prothrombotic endothelial dysfunction in COVID-19 #MMPMID34506304 Schmaier AA; Pajares Hurtado GM; Manickas-Hill ZJ; Sack KD; Chen SM; Bhambhani V; Quadir J; Nath AK; Collier AY; Ngo D; Barouch DH; Shapiro NI; Gerszten RE; Yu XG; Peters KG; Flaumenhaft R; Parikh SM JCI Insight 2021[Oct]; 6 (20): ä PMID34506304show ga Endothelial dysfunction accompanies the microvascular thrombosis commonly observed in severe COVID-19. Constitutively, the endothelial surface is anticoagulant, a property maintained at least in part via signaling through the Tie2 receptor. During inflammation, the Tie2 antagonist angiopoietin-2 (Angpt-2) is released from endothelial cells and inhibits Tie2, promoting a prothrombotic phenotypic shift. We sought to assess whether severe COVID-19 is associated with procoagulant endothelial dysfunction and alterations in the Tie2/angiopoietin axis. Primary HUVECs treated with plasma from patients with severe COVID-19 upregulated the expression of thromboinflammatory genes, inhibited the expression of antithrombotic genes, and promoted coagulation on the endothelial surface. Pharmacologic activation of Tie2 with the small molecule AKB-9778 reversed the prothrombotic state induced by COVID-19 plasma in primary endothelial cells. Lung autopsies from patients with COVID-19 demonstrated a prothrombotic endothelial signature. Assessment of circulating endothelial markers in a cohort of 98 patients with mild, moderate, or severe COVID-19 revealed endothelial dysfunction indicative of a prothrombotic state. Angpt-2 concentrations rose with increasing disease severity, and the highest levels were associated with worse survival. These data highlight the disruption of Tie2/angiopoietin signaling and procoagulant changes in endothelial cells in severe COVID-19. Our findings provide rationale for current trials of Tie2-activating therapy with AKB-9778 in COVID-19. |*COVID-19 Drug Treatment[MESH] |Adult[MESH] |Aged[MESH] |Aged, 80 and over[MESH] |Angiopoietin-2/metabolism[MESH] |Aniline Compounds[MESH] |Endothelial Cells/*drug effects[MESH] |Female[MESH] |Gene Expression[MESH] |Humans[MESH] |Lung[MESH] |Male[MESH] |Middle Aged[MESH] |Protective Agents/*pharmacology[MESH] |Receptor, TIE-2/genetics/*metabolism[MESH] |SARS-CoV-2[MESH] |Signal Transduction[MESH] |Sulfonic Acids[MESH] |Vascular Diseases/metabolism[MESH]Tie2 activation protects against prothrombotic endothelial dysfunction(epmc).pdf DeepDyve Pubget Overpricing