Literature DB >> 15920034

Impaired revascularization in a mouse model of type 2 diabetes is associated with dysregulation of a complex angiogenic-regulatory network.

Stephan Schiekofer1, Gennaro Galasso, Kaori Sato, Benjamin J Kraus, Kenneth Walsh.   

Abstract

OBJECTIVE: Diabetes is a risk factor for the development of cardiovascular diseases associated with impaired angiogenesis or increased endothelial cell apoptosis. METHODS AND
RESULTS: Here it is shown that angiogenic repair of ischemic hindlimbs was impaired in Lepr(db/db) mice, a leptin receptor-deficient model of diabetes, compared with wild-type (WT) C57BL/6 mice, as evaluated by laser Doppler flow and capillary density analyses. To identify molecular targets associated with this disease process, hindlimb cDNA expression profiles were created from adductor muscle of Lepr(db/db) and WT mice before and after hindlimb ischemia using Affymetrix GeneChip Mouse Expression Set microarrays. The expression patterns of numerous angiogenesis-related proteins were altered in Lepr(db/db) versus WT mice after ischemic injury. These transcripts included neuropilin-1, vascular endothelial growth factor-A, placental growth factor, elastin, and matrix metalloproteinases implicated in blood vessel growth and maintenance of vessel wall integrity.
CONCLUSIONS: These data illustrate that impaired ischemia-induced neovascularization in type 2 diabetes is associated with the dysregulation of a complex angiogenesis-regulatory network.

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Year:  2005        PMID: 15920034     DOI: 10.1161/01.ATV.0000171994.89106.ca

Source DB:  PubMed          Journal:  Arterioscler Thromb Vasc Biol        ISSN: 1079-5642            Impact factor:   8.311


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