Hdl Handle:
http://hdl.handle.net/10675.2/575
Title:
Adaptive Cerebral Neovascularization in a Model of Type 2 Diabetes
Authors:
Schreihofer, Derek A.; Fagan, Susan C.; Ergul, Adviye; Li, Weiguo; Prakash, Roshini; Kelley-Cobbs, Aisha I.; Ogbi, Safia; Kozak, Anna; El-Remessy, Azza B. ( 0000-0003-4386-1989 )
Abstract:
OBJECTIVE: The effect of diabetes on neovascularization varies between different organ systems. While excessive angiogenesis complicates diabetic retinopathy, impaired neovascularization contributes to coronary and peripheral complications of diabetes. However, how diabetes influences cerebral neovascularization is not clear. Our aim was to determine diabetes-mediated changes in the cerebrovasculature and its impact on the short-term outcome of cerebral ischemia.; RESEARCH DESIGN AND METHODS: Angiogenesis (capillary density) and arteriogenesis (number of collaterals and intratree anostomoses) were determined as indexes of neovascularization in the brain of control and type 2 diabetic Goto-Kakizaki (GK) rats. The infarct volume, edema, hemorrhagic transformation, and short-term neurological outcome were assessed after permanent middleâ cerebral artery occlusion (MCAO).; RESULTS: The number of collaterals between middle and anterior cerebral arteries, the anastomoses within middleâ cerebral artery trees, the vessel density, and the level of brain-derived neurotrophic factor were increased in diabetes. Cerebrovascular permeability, matrix metalloproteinase (MMP)-9 protein level, and total MMP activity were augmented while occludin was decreased in isolated cerebrovessels of the GK group. Following permanent MCAO, infarct size was smaller, edema was greater, and there was no macroscopic hemorrhagic transformation in GK rats.; CONCLUSIONS: The augmented neovascularization in the GK model includes both angiogenesis and arteriogenesis. While adaptive arteriogenesis of the pial vessels and angiogenesis at the capillary level may contribute to smaller infarction, changes in the tight junction proteins may lead to the greater edema following cerebral ischemia in diabetes.
Citation:
Diabetes. 2010 Jan 6; 59(1):228-235
Issue Date:
Jan-2010 ; 6-Oct-2009
URI:
http://hdl.handle.net/10675.2/575
DOI:
10.2337/db09-0902
PubMed ID:
19808897
PubMed Central ID:
PMC2797926
Type:
Article
ISSN:
1939-327X
Appears in Collections:
Department of Physiology: Faculty Research and Presentations

Full metadata record

DC FieldValue Language
dc.contributor.authorSchreihofer, Derek A.-
dc.contributor.authorFagan, Susan C.-
dc.contributor.authorErgul, Adviye-
dc.contributor.authorLi, Weiguoen_US
dc.contributor.authorPrakash, Roshinien_US
dc.contributor.authorKelley-Cobbs, Aisha I.en_US
dc.contributor.authorOgbi, Safiaen_US
dc.contributor.authorKozak, Annaen_US
dc.contributor.authorEl-Remessy, Azza B.en_US
dc.date.accessioned2012-10-26T16:26:46Z-
dc.date.available2012-10-26T16:26:46Z-
dc.date.issued2010-01en_US
dc.date.issued2009-10-6en_US
dc.identifier.citationDiabetes. 2010 Jan 6; 59(1):228-235en_US
dc.identifier.issn1939-327Xen_US
dc.identifier.pmid19808897en_US
dc.identifier.doi10.2337/db09-0902en_US
dc.identifier.urihttp://hdl.handle.net/10675.2/575-
dc.description.abstractOBJECTIVE: The effect of diabetes on neovascularization varies between different organ systems. While excessive angiogenesis complicates diabetic retinopathy, impaired neovascularization contributes to coronary and peripheral complications of diabetes. However, how diabetes influences cerebral neovascularization is not clear. Our aim was to determine diabetes-mediated changes in the cerebrovasculature and its impact on the short-term outcome of cerebral ischemia.en_US
dc.description.abstractRESEARCH DESIGN AND METHODS: Angiogenesis (capillary density) and arteriogenesis (number of collaterals and intratree anostomoses) were determined as indexes of neovascularization in the brain of control and type 2 diabetic Goto-Kakizaki (GK) rats. The infarct volume, edema, hemorrhagic transformation, and short-term neurological outcome were assessed after permanent middleâ cerebral artery occlusion (MCAO).en_US
dc.description.abstractRESULTS: The number of collaterals between middle and anterior cerebral arteries, the anastomoses within middleâ cerebral artery trees, the vessel density, and the level of brain-derived neurotrophic factor were increased in diabetes. Cerebrovascular permeability, matrix metalloproteinase (MMP)-9 protein level, and total MMP activity were augmented while occludin was decreased in isolated cerebrovessels of the GK group. Following permanent MCAO, infarct size was smaller, edema was greater, and there was no macroscopic hemorrhagic transformation in GK rats.en_US
dc.description.abstractCONCLUSIONS: The augmented neovascularization in the GK model includes both angiogenesis and arteriogenesis. While adaptive arteriogenesis of the pial vessels and angiogenesis at the capillary level may contribute to smaller infarction, changes in the tight junction proteins may lead to the greater edema following cerebral ischemia in diabetes.en_US
dc.rights© 2010 by the American Diabetes Association.en_US
dc.subjectOriginal Articleen_US
dc.subjectComplicationsen_US
dc.titleAdaptive Cerebral Neovascularization in a Model of Type 2 Diabetesen_US
dc.typeArticleen_US
dc.identifier.pmcidPMC2797926en_US
dc.contributor.corporatenameDepartment of Physiology-
dc.contributor.corporatenameDepartment of Neurology-

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