Mice that lack the angiogenesis inhibitor, thrombospondin 2, mount an altered foreign body reaction characterized by increased vascularity.
about
Thrombospondin 2 inhibits microvascular endothelial cell proliferation by a caspase-independent mechanism.Thrombospondin-2 plays a protective role in multistep carcinogenesis: a novel host anti-tumor defense mechanism.Tendon development and musculoskeletal assembly: emerging roles for the extracellular matrixMolecular Characterization of Macrophage-Biomaterial InteractionsBiomaterials as carrier, barrier and reactor for cell-based regenerative medicineThrombospondin type 1 repeats interact with matrix metalloproteinase 2. Regulation of metalloproteinase activityControl of in vivo microvessel ingrowth by modulation of biomaterial local architecture and chemistryDelineation of candidate genes responsible for structural brain abnormalities in patients with terminal deletions of chromosome 6q27Matricellular proteins and biomaterials.Dynamics of cardiac wound healing following myocardial infarction: observations in genetically altered mice.Matricellular proteins as modulators of cell-matrix interactions: adhesive defect in thrombospondin 2-null fibroblasts is a consequence of increased levels of matrix metalloproteinase-2.Up-regulation of thrombospondin-2 in Akt1-null mice contributes to compromised tissue repair due to abnormalities in fibroblast function.Cervical softening during pregnancy: regulated changes in collagen cross-linking and composition of matricellular proteins in the mouse.Long-term gene therapy with thrombospondin 2 inhibits TGF-β activation, inflammation and angiogenesis in chronic allograft nephropathyMatricellular homologs in the foreign body response: hevin suppresses inflammation, but hevin and SPARC together diminish angiogenesis.Thrombospondin 2 functions as an endogenous regulator of angiogenesis and inflammation in rheumatoid arthritis.The CC chemokine ligand, CCL2/MCP1, participates in macrophage fusion and foreign body giant cell formation.The thrombospondins.Revisiting the matricellular concept.Endothelial nitric oxide synthase controls the expression of the angiogenesis inhibitor thrombospondin 2Thrombospondin-2 Expression During Retinal Vascular Development and Neovascularization.Profiles of carbohydrate ligands associated with adsorbed proteins on self-assembled monolayers of defined chemistries.Bioactive nanofibers enable the identification of thrombospondin 2 as a key player in enamel regeneration.Manipulating angiogenesis in medicine.Altered extracellular matrix remodeling and angiogenesis in sponge granulomas of thrombospondin 2-null miceCompromised production of extracellular matrix in mice lacking secreted protein, acidic and rich in cysteine (SPARC) leads to a reduced foreign body reaction to implanted biomaterials.Role of plasma fibronectin in the foreign body response to biomaterialsLack of thrombospondin-2 reduces fibrosis and increases vascularity around cardiac cell grafts.Matricellular proteins in drug delivery: Therapeutic targets, active agents, and therapeutic localizationExtracellular matrix-based biomaterial scaffolds and the host response.Thrombospondin-2: a potent endogenous inhibitor of tumor growth and angiogenesis.Inadequate Processing of Decellularized Dermal Matrix Reduces Cell Viability In Vitro and Increases Apoptosis and Acute Inflammation In Vivo.Macrophage fusion, giant cell formation, and the foreign body response require matrix metalloproteinase 9.Enhanced angiogenesis and reduced contraction in thrombospondin-2-null wounds is associated with increased levels of matrix metalloproteinases-2 and -9, and soluble VEGF.Thrombospondin 2-null mice display an altered brain foreign body response to polyvinyl alcohol sponge implantsGene silencing in human aortic smooth muscle cells induced by PEI-siRNA complexes released from dip-coated electrospun poly(ethylene terephthalate) grafts.The role of thrombospondins in wound healing, ischemia, and the foreign body reaction.Thrombospondin-2 overexpression in the skin of transgenic mice reduces the susceptibility to chemically induced multistep skin carcinogenesisBiomimetic coatings for bone tissue engineering of critical-sized defectsThrombospondin-2 and extracellular matrix assembly.
P2860
Q24531386-BF2F2AA5-119A-4688-B622-676C3532D107Q24535504-239D0F66-1F20-4E49-9FFE-944196CC44D9Q26775671-C8145661-DFCC-4DA0-8842-76A052031D34Q26797412-C6B4F450-CFD7-401D-A940-2BB434C62CF3Q28083709-CC308CD7-6CC1-4013-AA15-E6ADE1862CA5Q28141127-3367610F-D072-40A1-B076-72E4D4DE1B74Q28576917-0B89D6EC-6E82-4E84-BC32-3163B666BE45Q30801843-4B10B267-6B2C-4114-AD00-C9DCFB9CE9A9Q34040283-42481BD7-42AD-4CA0-9F36-22C54F7ACE2DQ34418975-C3EE604A-A349-4DC4-9F2D-EABB65424E87Q34763728-67DF875E-6D25-455A-91B0-38C87BB9761DQ34801542-120D8A3B-66C3-4F5E-94C2-11B2AECA1C94Q34827041-D5BFB22B-3433-4EC9-8FB6-827333728618Q35078258-387574DC-460A-49E6-8017-94A58E3F0272Q35083699-18CA42F9-581A-4CC7-8306-7B9CCB676B6FQ35103501-2E564095-9C8A-48D5-B9AC-0845B2D7F1A0Q35103605-3A77069E-1B00-4417-84AB-38248A47083BQ35230013-32AB7B4F-03F8-4525-A6EC-F916AE582269Q35233858-6A6643B4-FE73-4F04-BC8F-123ADB5E4999Q35558854-2D241778-263C-40A9-B502-F78357E77F47Q35623995-50751F25-8E03-41A0-A8E9-DA88B10DEA63Q35678201-417B67EC-2816-452A-A01E-99288F80ABC1Q35742861-FEFC3EEB-421F-4B60-9617-83E791F871A0Q35743851-EA5BC136-3357-49AB-9ABE-2A3A0664D392Q35746911-D795E9EB-8CB7-47CF-A650-A555A7CAB31BQ35748929-70A4BDBB-A991-4A9E-8E69-4D52016B5FACQ35945230-64AC1127-946C-4134-B497-BEA75695AB88Q36106627-C011CBC3-120E-4886-9E2B-64AF26F8B4C6Q36578825-C30A04C9-0AB0-411E-8158-1590C600C2A3Q36669532-79FC3637-096F-443B-AB9B-AF3814EFF0C4Q36775071-E88FCB13-18D9-49A4-BC52-D90AAE487AE2Q37102049-828BF832-5CAF-472E-8E23-1C8C40DA0F3AQ37130179-D1110405-E799-4C96-B750-FA1F70A85BDCQ37149361-84B0EEBA-F8A0-4C9F-9351-D27C6BD087CCQ37171093-2627C79F-39BA-4050-89DE-C74E1343BA76Q37593277-1132E373-669B-4F53-B739-7829B9388062Q37618614-A086D1E2-EBD3-44E2-AC13-C043BF2B7170Q37684615-85975929-596A-49DF-97FC-7592FBC20062Q37756361-7BA12AF9-0496-4A46-BD60-A7BC120010FDQ38179711-FAC7DAEF-A372-4A25-B99B-4A2090CBCF93
P2860
Mice that lack the angiogenesis inhibitor, thrombospondin 2, mount an altered foreign body reaction characterized by increased vascularity.
description
1999 nî lūn-bûn
@nan
1999 թուականի Ապրիլին հրատարակուած գիտական յօդուած
@hyw
1999 թվականի ապրիլին հրատարակված գիտական հոդված
@hy
1999年の論文
@ja
1999年論文
@yue
1999年論文
@zh-hant
1999年論文
@zh-hk
1999年論文
@zh-mo
1999年論文
@zh-tw
1999年论文
@wuu
name
Mice that lack the angiogenesi ...... ized by increased vascularity.
@ast
Mice that lack the angiogenesi ...... ized by increased vascularity.
@en
type
label
Mice that lack the angiogenesi ...... ized by increased vascularity.
@ast
Mice that lack the angiogenesi ...... ized by increased vascularity.
@en
prefLabel
Mice that lack the angiogenesi ...... ized by increased vascularity.
@ast
Mice that lack the angiogenesi ...... ized by increased vascularity.
@en
P2093
P2860
P356
P1476
Mice that lack the angiogenesi ...... ized by increased vascularity.
@en
P2093
A S Hoffman
B D Ratner
P Bornstein
T R Kyriakides
P2860
P304
P356
10.1073/PNAS.96.8.4449
P407
P577
1999-04-01T00:00:00Z