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Functional heterogeneity in vascular remodeling (MMP‐9−/− and PAR‐1−/+) in hyperhomocysteinemic (CBS‐/+) and diabetic (Akita, Ins2−/+) mice.
Author(s) -
Givvimani Srikanth,
Jala Ramanjamma,
Mishra Paras Kumar,
Sen Utpal,
Tyagi Neetu,
Qipshidze Natia,
Munjal Charu,
Kandel Madhavi,
Tyagi Suresh.C
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.599.6
Subject(s) - medicine , endocrinology , hyperhomocysteinemia , diabetes mellitus , homocysteine
Although proteinase activated receptor‐1 (PAR‐1) and matrix metalloproteinase‐9 (MMP‐9) play significant role in vasculogenesis and remodeling in hyperhomocysteinemia (HHcy) and diabetes, the mechanism remains nebulous. To test the hypothesis that differential vasculogenesis and remodeling in different vascular beds in hyperhomocysteinemia and diabetes was an adaptive phenomenon during pathogenesis, we measured vascular density in heart, lung, liver, kidney, intestinal mesentery and brain of mice lacking PAR‐1, MMP‐9, CBS and Insulin‐2 gene(Ins2), and compared with wild type C57Bl/6J mice. The vascular density was detected by X‐ray angiography using KODAK 4000 MM image station by infusing barium sulfate solution through carotid artery and jugular vein at constant flow rate of 200 micro.lit/min for 5 min using syringe pump. Coronary vascular density in the hearts of CBS−/+ (HHcy) and Ins2−/+ (Akita, type‐1 diabetic mice) was decreased while lung vasculature was increased in CBS−/+ and MMP‐9−/−. There was decrease in vascular density in liver and renal vasculature of CBS−/+ and Akita mice. Vascular density in brain and intestinal mesentery was decreased in CBS−/+ mice. Collectively these findings suggest that metabolic derangement in diabetes and hyperhomocysteinemia caused chronic decline/rarefaction in vasculature.