{"@type": "dcat:Dataset", "accessLevel": "public", "bureauCode": ["009:25"], "contactPoint": {"@type": "vcard:Contact", "fn": "NIH", "hasEmail": "mailto:info@nih.gov"}, "description": "The matricellular protein thrombospondin 2 (TSP2) regulates a\nvariety of cell\u2013matrix interactions. A prominent feature of TSP2-null\nmice is increased microvascular density, particularly in connective\ntissues synthesized after injury. We investigated the cellular basis\nfor the regulation of angiogenesis by TSP2 in cultures of murine and\nhuman fibroblasts and endothelial cells. Fibroblasts isolated from\nmurine and human dermis synthesize TSP2 mRNA and secrete significant\namounts of immunoreactive TSP2, whereas endothelial cells from mouse\nlung and human dermis did not synthesize TSP2 mRNA or protein.\nRecombinant mouse TSP2 inhibited growth of human microvascular\nendothelial cells (HMVECs) mediated by basic fibroblast growth factor,\ninsulin-like growth factor-1, epidermal growth factor, and vascular\nendothelial growth factor (VEGF). HMVECs exposed to TSP2 in the\npresence of these growth factors had a decreased proportion of cells in\nS and G2/M phases. HMVECs cultured with a combination of\nbasic fibroblast growth factor, insulin-like growth factor-1, and\nepidermal growth factor displayed an increased proportion of nonviable\ncells in the presence of TSP2, but the addition of VEGF blocked this\nTSP2-mediated impairment of cell viability. TSP2-mediated inhibition of\nDNA synthesis by HMVECs in the presence of VEGF was not affected by the\nbroad-spectrum caspase inhibitor zVAD-fmk. Similar findings were\nobtained with TSP1. Taken together, these observations indicate that\neither TSP2 or TSP1 can inhibit HMVEC proliferation by inhibition of\ncell cycle progression and induction of cell death, but the mechanisms\nresponsible for TSP2-mediated inhibition of cell cycle progression are\nindependent from those leading to cell death.", "distribution": [{"@type": "dcat:Distribution", "description": "Visit the original government dataset for complete information, documentation, and data access.", "downloadURL": "https://www.ncbi.nlm.nih.gov/pmc/articles/PMC117612/", "mediaType": "text/html", "title": "Official Government Data Source"}], "identifier": "https://healthdata.gov/api/views/q3a7-8dmm", "issued": "2025-07-14", "keyword": ["angiogenesis-inhibition", "endothelial-cell-proliferation", "microvascular-density", "nih", "thrombospondin-2"], "landingPage": "https://healthdata.gov/d/q3a7-8dmm", "modified": "2025-09-06", "programCode": ["009:033"], "publisher": {"@type": "org:Organization", "name": "National Institutes of Health"}, "theme": ["NIH"], "title": "Thrombospondin 2 Inhibits Microvascular Endothelial Cell\nProliferation by a Caspase-independent Mechanism"}