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10.1074/jbc.M114.557835 http://scihub22266oqcxt.onion/10.1074/jbc.M114.557835 C4175356!4175356 !25100725     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=25100725 &cmd=llinks): Failed to open stream: HTTP request failed! 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Vildagliptin stimulates endothelial cell network formation and ischemia-induced revascularization via an endothelial nitric-oxide synthase-dependent mechanism |pdf=|usr=}}{{25100725 }} gab.com Text Vildagliptin stimulates endothelial cell network formation and ischemia-induced revascularization via an endothelial nitric-oxide synthase-dependent mechanism JO: J Biol Chem http://www.kidney.de/pget.php?&tw=1&pmid=25100725 #FOAvip Dipeptidyl peptidase-4 inhibitors are known to lower glucose levels and are also beneficial in the management of cardiovascular disease. Here, we investigated whether a dipeptidyl peptidase-4 inhibitor, vildagliptin, modulates endothelial cell network formation and revascularization processes in vitro and in vivo. Treatment with vildagliptin enhanced blood flow recovery and capillary density in the ischemic limbs of wild-type mice, with accompanying increases in phosphorylation of Akt and endothelial nitric-oxide synthase (eNOS). In contrast to wild-type mice, treatment with vildagliptin did not improve blood flow in ischemic muscles of eNOS-deficient mice. Treatment with vildagliptin increased the levels of glucagon-like peptide-1 (GLP-1) and adiponectin, which have protective effects on the vasculature. Both vildagliptin and GLP-1 increased the differentiation of cultured human umbilical vein endothelial cells (HUVECs) into vascular-like structures, although vildagliptin was less effective than GLP-1. GLP-1 and vildagliptin also stimulated the phosphorylation of Akt and eNOS in HUVECs. Pretreatment with a PI3 kinase or NOS inhibitor blocked the stimulatory effects of both vildagliptin and GLP-1 on HUVEC differentiation. Furthermore, treatment with vildagliptin only partially increased the limb flow of ischemic muscle in adiponectin-deficient mice in vivo. GLP-1, but not vildagliptin, significantly increased adiponectin expression in differentiated 3T3-L1 adipocytes in vitro. These data indicate that vildagliptin promotes endothelial cell function via eNOS signaling, an effect that may be mediated by both GLP-1-dependent and GLP-1-independent mechanisms. The beneficial activity of GLP-1 for revascularization may also be partially mediated by its ability to increase adiponectin production. Twit Text FOAVip Vildagliptin stimulates endothelial cell network formation and ischemia-induced revascularization via an endothelial nitric-oxide synthase-dependent mechanism ????J Biol Chem http://www.kidney.de/pget.php?&tw=1&pmid=25100725 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25100725 #FOAvip English Wikipedia <ref>{{Cite pmid|25100725 }}</ref> Vildagliptin stimulates endothelial cell network formation and ischemia-induced revascularization via an endothelial nitric-oxide synthase-dependent mechanism #MMPMID25100725 Ishii M ; Shibata R ; Kondo K ; Kambara T ; Shimizu Y ; Tanigawa T ; Bando YK ; Nishimura M ; Ouchi N ; Murohara T J Biol Chem 2014[Sep]; 289 (39 ): 27235-27245 PMID25100725 show ga Dipeptidyl peptidase-4 inhibitors are known to lower glucose levels and are also beneficial in the management of cardiovascular disease. Here, we investigated whether a dipeptidyl peptidase-4 inhibitor, vildagliptin, modulates endothelial cell network formation and revascularization processes in vitro and in vivo. Treatment with vildagliptin enhanced blood flow recovery and capillary density in the ischemic limbs of wild-type mice, with accompanying increases in phosphorylation of Akt and endothelial nitric-oxide synthase (eNOS). In contrast to wild-type mice, treatment with vildagliptin did not improve blood flow in ischemic muscles of eNOS-deficient mice. Treatment with vildagliptin increased the levels of glucagon-like peptide-1 (GLP-1) and adiponectin, which have protective effects on the vasculature. Both vildagliptin and GLP-1 increased the differentiation of cultured human umbilical vein endothelial cells (HUVECs) into vascular-like structures, although vildagliptin was less effective than GLP-1. GLP-1 and vildagliptin also stimulated the phosphorylation of Akt and eNOS in HUVECs. Pretreatment with a PI3 kinase or NOS inhibitor blocked the stimulatory effects of both vildagliptin and GLP-1 on HUVEC differentiation. Furthermore, treatment with vildagliptin only partially increased the limb flow of ischemic muscle in adiponectin-deficient mice in vivo. GLP-1, but not vildagliptin, significantly increased adiponectin expression in differentiated 3T3-L1 adipocytes in vitro. These data indicate that vildagliptin promotes endothelial cell function via eNOS signaling, an effect that may be mediated by both GLP-1-dependent and GLP-1-independent mechanisms. The beneficial activity of GLP-1 for revascularization may also be partially mediated by its ability to increase adiponectin production. |*Neovascularization, Physiologic [MESH] |*Signal Transduction [MESH] |3T3-L1 Cells [MESH] |Adamantane/*analogs & derivatives/pharmacology [MESH] |Adipocytes/metabolism [MESH] |Adiponectin/metabolism [MESH] |Animals [MESH] |Cell Differentiation [MESH] |Dipeptidyl-Peptidase IV Inhibitors/*pharmacology [MESH] |Glucagon-Like Peptide 1/metabolism [MESH] |Hindlimb/blood supply/metabolism [MESH] |Human Umbilical Vein Endothelial Cells/*metabolism [MESH] |Ischemia/*metabolism [MESH] |Mice [MESH] |Mice, Knockout [MESH] |Muscle, Skeletal/blood supply/*metabolism [MESH] |Nitric Oxide Synthase Type III/*metabolism [MESH] |Nitriles/*pharmacology [MESH] |Phosphatidylinositol 3-Kinases/metabolism [MESH] |Proto-Oncogene Proteins c-akt/metabolism [MESH] |Pyrrolidines/*pharmacology [MESH]Vildagliptin stimulates endothelial cell network formation and ischemi(epmc).pdf DeepDyve Pubget Overpricing