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10.1111/j.1582-4934.2008.00555.x http://scihub22266oqcxt.onion/10.1111/j.1582-4934.2008.00555.x C4515065!4515065 !19602055     free     free     free Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 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\19602055 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       J+Cell+Mol+Med 2009 ; 13 (11-12 ): 4492-504 Nephropedia Template TP {{tp|p=19602055 |t=2009. Cell and molecular mechanisms of insulin-induced angiogenesis |pdf=|usr=}}{{19602055 }} gab.com Text Cell and molecular mechanisms of insulin-induced angiogenesis JO: J Cell Mol Med http://www.kidney.de/pget.php?&tw=1&pmid=19602055 #FOAvip Angiogenesis, the development of new blood vessel from pre-existing vessels, is a key process in the formation of the granulation tissue during wound healing. The appropriate development of new blood vessels, along with their subsequent maturation and differentiation, establishes the foundation for functional wound neovasculature. We performed studies in vivo and used a variety of cellular and molecular approaches in vitro to show that insulin stimulates angiogenesis and to elucidate the signalling mechanisms by which this protein stimulates microvessel development. Mice skin injected with insulin shows longer vessels with more branches, along with increased numbers of associated alpha-smooth muscle actin-expressing cells, suggesting the appropriate differentiation and maturation of the new vessels. We also found that insulin stimulates human microvascular endothelial cell migration and tube formation, and that these effects occur independently of VEGF/VEGFR signalling, but are dependent upon the insulin receptor itself. Downstream signalling pathways involve PI3K, Akt, sterol regulatory element-binding protein 1 (SREBP-1) and Rac1; inhibition of these pathways results in elimination of endothelial cell migration and tube formation and significantly decreases the development of microvessels. Our findings strongly suggest that insulin is a good candidate for the treatment of ischaemic wounds and other conditions in which blood vessel development is impaired. Twit Text FOAVip Cell and molecular mechanisms of insulin-induced angiogenesis ????J Cell Mol Med http://www.kidney.de/pget.php?&tw=1&pmid=19602055 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=19602055 #FOAvip English Wikipedia <ref>{{Cite pmid|19602055 }}</ref> Cell and molecular mechanisms of insulin-induced angiogenesis #MMPMID19602055 Liu Y ; Petreaca M ; Martins-Green M J Cell Mol Med 2009[Nov]; 13 (11-12 ): 4492-504 PMID19602055 show ga Angiogenesis, the development of new blood vessel from pre-existing vessels, is a key process in the formation of the granulation tissue during wound healing. The appropriate development of new blood vessels, along with their subsequent maturation and differentiation, establishes the foundation for functional wound neovasculature. We performed studies in vivo and used a variety of cellular and molecular approaches in vitro to show that insulin stimulates angiogenesis and to elucidate the signalling mechanisms by which this protein stimulates microvessel development. Mice skin injected with insulin shows longer vessels with more branches, along with increased numbers of associated alpha-smooth muscle actin-expressing cells, suggesting the appropriate differentiation and maturation of the new vessels. We also found that insulin stimulates human microvascular endothelial cell migration and tube formation, and that these effects occur independently of VEGF/VEGFR signalling, but are dependent upon the insulin receptor itself. Downstream signalling pathways involve PI3K, Akt, sterol regulatory element-binding protein 1 (SREBP-1) and Rac1; inhibition of these pathways results in elimination of endothelial cell migration and tube formation and significantly decreases the development of microvessels. Our findings strongly suggest that insulin is a good candidate for the treatment of ischaemic wounds and other conditions in which blood vessel development is impaired. |Animals [MESH] |Cell Line [MESH] |Cell Membrane/drug effects/enzymology [MESH] |Cell Movement/drug effects [MESH] |Cell Proliferation/drug effects [MESH] |Endothelial Cells/cytology/drug effects/enzymology [MESH] |Humans [MESH] |Injections, Subcutaneous [MESH] |Insulin/administration & dosage/*pharmacology [MESH] |Mice [MESH] |Mice, Inbred C57BL [MESH] |Microvessels/cytology/drug effects [MESH] |Neovascularization, Physiologic/*drug effects [MESH] |Phosphatidylinositol 3-Kinases/metabolism [MESH] |Protein Transport/drug effects [MESH] |Proto-Oncogene Proteins c-akt/metabolism [MESH] |Receptor, Insulin/metabolism [MESH] |Signal Transduction/drug effects [MESH] |Skin/blood supply/drug effects [MESH] |Sterol Regulatory Element Binding Protein 1/metabolism [MESH] |Time Factors [MESH]Cell and molecular mechanisms of insulin-induced angiogenesis (epmc).pdf DeepDyve Pubget Overpricing