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10.1161/CIRCRESAHA.116.309754 http://scihub22266oqcxt.onion/10.1161/CIRCRESAHA.116.309754 C5446274!5446274!28325782     free     free     free Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Circ+Res 2017 ; 120 (11): 1727-39 Nephropedia Template TP {{tp|p=28325782|t=2017. AIBP Limits Angiogenesis Through ?-Secretase-Mediated Upregulation of Notch Signaling |pdf=|usr=}}{{28325782}} gab.com Text AIBP Limits Angiogenesis Through -Secretase-Mediated Upregulation of Notch Signaling JO: Circ Res http://www.kidney.de/pget.php?&tw=1&pmid=28325782 #FOAvip Rationale: Angiogenesis improves perfusion to the ischemic tissue following acute vascular obstruction. Angiogenesis in pathophysiological settings reactivates signaling pathways involved in developmental angiogenesis. We showed previously that apoA-I binding protein (AIBP)-regulated cholesterol efflux in endothelial cells (ECs) controls zebrafish embryonic angiogenesis. Objective: This study is to determine whether loss of AIBP affects angiogenesis in mice during development and under pathological conditions, and to explore the underlying molecular mechanism. Methods and Results: In this paper, we report the generation of AIBP knockout (Apoa1bp?/?) mice, which are characterized of accelerated postnatal retinal angiogenesis. Mechanistically, AIBP triggered relocalization of ?-secretase from lipid rafts to non-lipid rafts where it cleaved Notch. Consistently, AIBP treatment enhanced DLL4-stimulated Notch activation in human retinal ECs. Increasing HDL levels in Apoa1bp?/? mice by crossing them with apoA-I transgenic mice rescued Notch activation and corrected dysregulated retinal angiogenesis. Notably, the retinal vessels in Apoa1bp?/? mice manifested normal pericyte coverage and vascular integrity. Similarly, in the subcutaneous Matrigel plug assay, which mimics ischemic/inflammatory neovascularization, angiogenesis was dramatically upregulated in Apoa1bp?/? mice and associated with a profound inhibition of Notch activation and reduced expression of downstream targets. Furthermore, loss of AIBP increased vascular density and facilitated the recovery of blood vessel perfusion function in a murine hindlimb ischemia model. In addition, AIBP expression was significantly increased in human patients with ischemic cardiomyopathy. Conclusions: Our data reveal a novel mechanistic connection between AIBP-mediated cholesterol metabolism and Notch signaling, implicating AIBP as a possible druggable target to modulate angiogenesis under pathological conditions. Twit Text FOAVip AIBP Limits Angiogenesis Through -Secretase-Mediated Upregulation of Notch Signaling ????Circ Res http://www.kidney.de/pget.php?&tw=1&pmid=28325782 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28325782 #FOAvip English Wikipedia <ref>{{Cite pmid|28325782}}</ref> AIBP Limits Angiogenesis Through ?-Secretase-Mediated Upregulation of Notch Signaling #MMPMID28325782 Mao R; Meng S; Gu Q; Araujo-Gutierrez R; Kumar S; Yan Q; Almazan F; Youker KA; Fu Y; Pownall HJ; Cooke JP; Miller YI; Fang L Circ Res 2017[May]; 120 (11): 1727-39 PMID28325782show ga Rationale: Angiogenesis improves perfusion to the ischemic tissue following acute vascular obstruction. Angiogenesis in pathophysiological settings reactivates signaling pathways involved in developmental angiogenesis. We showed previously that apoA-I binding protein (AIBP)-regulated cholesterol efflux in endothelial cells (ECs) controls zebrafish embryonic angiogenesis. Objective: This study is to determine whether loss of AIBP affects angiogenesis in mice during development and under pathological conditions, and to explore the underlying molecular mechanism. Methods and Results: In this paper, we report the generation of AIBP knockout (Apoa1bp?/?) mice, which are characterized of accelerated postnatal retinal angiogenesis. Mechanistically, AIBP triggered relocalization of ?-secretase from lipid rafts to non-lipid rafts where it cleaved Notch. Consistently, AIBP treatment enhanced DLL4-stimulated Notch activation in human retinal ECs. Increasing HDL levels in Apoa1bp?/? mice by crossing them with apoA-I transgenic mice rescued Notch activation and corrected dysregulated retinal angiogenesis. Notably, the retinal vessels in Apoa1bp?/? mice manifested normal pericyte coverage and vascular integrity. Similarly, in the subcutaneous Matrigel plug assay, which mimics ischemic/inflammatory neovascularization, angiogenesis was dramatically upregulated in Apoa1bp?/? mice and associated with a profound inhibition of Notch activation and reduced expression of downstream targets. Furthermore, loss of AIBP increased vascular density and facilitated the recovery of blood vessel perfusion function in a murine hindlimb ischemia model. In addition, AIBP expression was significantly increased in human patients with ischemic cardiomyopathy. Conclusions: Our data reveal a novel mechanistic connection between AIBP-mediated cholesterol metabolism and Notch signaling, implicating AIBP as a possible druggable target to modulate angiogenesis under pathological conditions. äAIBP Limits Angiogenesis Through ?-Secretase-Mediated Upregulation of (epmc).pdf DeepDyve Pubget Overpricing