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10.1161/CIRCULATIONAHA.114.006614 http://scihub22266oqcxt.onion/10.1161/CIRCULATIONAHA.114.006614 C4190117!4190117 !25116956     free     free     free Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 267.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 267.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 267.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 267.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 267.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 300.79999999999995 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 300.79999999999995 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 300.79999999999995 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 300.79999999999995 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 300.79999999999995 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\25116956 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Circulation 2014 ; 130 (15 ): 1274-86 Nephropedia Template TP {{tp|p=25116956 |t=2014. Alternatively spliced tissue factor promotes plaque angiogenesis through the activation of hypoxia-inducible factor-1? and vascular endothelial growth factor signaling |pdf=|usr=}}{{25116956 }} gab.com Text Alternatively spliced tissue factor promotes plaque angiogenesis through the activation of hypoxia-inducible factor-1 and vascular endothelial growth factor signaling JO: Circulation http://www.kidney.de/pget.php?&tw=1&pmid=25116956 #FOAvip BACKGROUND: Alternatively spliced tissue factor (asTF) is a novel isoform of full-length tissue factor, which exhibits angiogenic activity. Although asTF has been detected in human plaques, it is unknown whether its expression in atherosclerosis causes increased neovascularization and an advanced plaque phenotype. METHODS AND RESULTS: Carotid (n=10) and coronary (n=8) specimens from patients with stable or unstable angina were classified as complicated or uncomplicated on the basis of plaque morphology. Analysis of asTF expression and cell type-specific expression revealed a strong expression and colocalization of asTF with macrophages and neovessels within complicated, but not uncomplicated, human plaques. Our results showed that the angiogenic activity of asTF is mediated via hypoxia-inducible factor-1? upregulation through integrins and activation of phosphatidylinositol-3-kinase/Akt and mitogen-activated protein kinase pathways. Hypoxia-inducible factor-1? upregulation by asTF also was associated with increased vascular endothelial growth factor expression in primary human endothelial cells, and vascular endothelial growth factor-Trap significantly reduced the angiogenic effect of asTF in vivo. Furthermore, asTF gene transfer significantly increased neointima formation and neovascularization after carotid wire injury in ApoE(-/-) mice. CONCLUSIONS: The results of this study provide strong evidence that asTF promotes neointima formation and angiogenesis in an experimental model of accelerated atherosclerosis. Here, we demonstrate that the angiogenic effect of asTF is mediated via the activation of the hypoxia-inducible factor-1/vascular endothelial growth factor signaling. This mechanism may be relevant to neovascularization and the progression and associated complications of human atherosclerosis as suggested by the increased expression of asTF in complicated versus uncomplicated human carotid and coronary plaques. Twit Text FOAVip Alternatively spliced tissue factor promotes plaque angiogenesis through the activation of hypoxia-inducible factor-1 and vascular endothelial growth factor signaling ????Circulation http://www.kidney.de/pget.php?&tw=1&pmid=25116956 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25116956 #FOAvip English Wikipedia <ref>{{Cite pmid|25116956 }}</ref> Alternatively spliced tissue factor promotes plaque angiogenesis through the activation of hypoxia-inducible factor-1? and vascular endothelial growth factor signaling #MMPMID25116956 Giannarelli C ; Alique M ; Rodriguez DT ; Yang DK ; Jeong D ; Calcagno C ; Hutter R ; Millon A ; Kovacic JC ; Weber T ; Faries PL ; Soff GA ; Fayad ZA ; Hajjar RJ ; Fuster V ; Badimon JJ Circulation 2014[Oct]; 130 (15 ): 1274-86 PMID25116956 show ga BACKGROUND: Alternatively spliced tissue factor (asTF) is a novel isoform of full-length tissue factor, which exhibits angiogenic activity. Although asTF has been detected in human plaques, it is unknown whether its expression in atherosclerosis causes increased neovascularization and an advanced plaque phenotype. METHODS AND RESULTS: Carotid (n=10) and coronary (n=8) specimens from patients with stable or unstable angina were classified as complicated or uncomplicated on the basis of plaque morphology. Analysis of asTF expression and cell type-specific expression revealed a strong expression and colocalization of asTF with macrophages and neovessels within complicated, but not uncomplicated, human plaques. Our results showed that the angiogenic activity of asTF is mediated via hypoxia-inducible factor-1? upregulation through integrins and activation of phosphatidylinositol-3-kinase/Akt and mitogen-activated protein kinase pathways. Hypoxia-inducible factor-1? upregulation by asTF also was associated with increased vascular endothelial growth factor expression in primary human endothelial cells, and vascular endothelial growth factor-Trap significantly reduced the angiogenic effect of asTF in vivo. Furthermore, asTF gene transfer significantly increased neointima formation and neovascularization after carotid wire injury in ApoE(-/-) mice. CONCLUSIONS: The results of this study provide strong evidence that asTF promotes neointima formation and angiogenesis in an experimental model of accelerated atherosclerosis. Here, we demonstrate that the angiogenic effect of asTF is mediated via the activation of the hypoxia-inducible factor-1/vascular endothelial growth factor signaling. This mechanism may be relevant to neovascularization and the progression and associated complications of human atherosclerosis as suggested by the increased expression of asTF in complicated versus uncomplicated human carotid and coronary plaques. |Alternative Splicing/*physiology [MESH] |Animals [MESH] |Apolipoproteins E/deficiency/genetics [MESH] |Carotid Arteries/pathology/physiopathology [MESH] |Coronary Vessels/pathology/physiopathology [MESH] |Disease Models, Animal [MESH] |Endothelium, Vascular/pathology/physiopathology [MESH] |Humans [MESH] |Hypoxia-Inducible Factor 1, alpha Subunit/*physiology [MESH] |Male [MESH] |Mice [MESH] |Mice, Inbred C57BL [MESH] |Neointima/physiopathology [MESH] |Neovascularization, Pathologic/*physiopathology [MESH] |Plaque, Atherosclerotic/pathology/*physiopathology [MESH] |Signal Transduction/*physiology [MESH] |Thromboplastin/*physiology [MESH] |Up-Regulation/physiology [MESH]Alternatively spliced tissue factor promotes plaque angiogenesis throu(epmc).pdf DeepDyve Pubget Overpricing