{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Gooz P"],"funding":["NCRR NIH HHS","NIDDK NIH HHS"],"pagination":["33-8"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC2875258"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["380(1)"],"pubmed_abstract":["Modulation of angiogenesis is a promising approach for treating a wide variety of human diseases including ischemic heart disease and cancer. In this study, we show that ADAM-17 is an important regulator of several key steps during angiogenesis. Knocking down ADAM-17 expression using lentivirus-delivered siRNA in HUVECs inhibited cell proliferation and the ability of cells to form close contact in two-dimensional cultures. Similarly, ADAM-17 depletion inhibited the ability of HUVECs to form capillary-like networks on top of three-dimensional Matrigel as well as in co-culture with fibroblasts within a three-dimensional scaffold. In mechanistic studies, both baseline and VEGF-induced MMP-2 activation and Matrigel invasion were inhibited by ADAM-17 depletion. Based on our findings we propose "],"journal":["Biochemical and biophysical research communications"],"pubmed_title":["ADAM-17 regulates endothelial cell morphology, proliferation, and in vitro angiogenesis."],"pmcid":["PMC2875258"],"funding_grant_id":["P20 RR016434-096032","K01 DK070054","P20 RR016434","K01 DK070054-05","K01 DK070054-01"],"pubmed_authors":["Gooz M","Gooz P","Baldys A","Hoffman S"],"additional_accession":[]},"is_claimable":false,"name":"ADAM-17 regulates endothelial cell morphology, proliferation, and in vitro angiogenesis.","description":"Modulation of angiogenesis is a promising approach for treating a wide variety of human diseases including ischemic heart disease and cancer. In this study, we show that ADAM-17 is an important regulator of several key steps during angiogenesis. Knocking down ADAM-17 expression using lentivirus-delivered siRNA in HUVECs inhibited cell proliferation and the ability of cells to form close contact in two-dimensional cultures. Similarly, ADAM-17 depletion inhibited the ability of HUVECs to form capillary-like networks on top of three-dimensional Matrigel as well as in co-culture with fibroblasts within a three-dimensional scaffold. In mechanistic studies, both baseline and VEGF-induced MMP-2 activation and Matrigel invasion were inhibited by ADAM-17 depletion. Based on our findings we propose ","dates":{"release":"2009-01-01T00:00:00Z","publication":"2009 Feb","modification":"2025-04-21T16:59:07.552Z","creation":"2019-06-06T22:07:27Z"},"accession":"S-EPMC2875258","cross_references":{"pubmed":["19150341"],"doi":["10.1016/j.bbrc.2009.01.013"]}}