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Connexin expression after femoral artery ligation
Author(s) -
Ambrecht Lindsay,
LooftWilson Robin
Publication year - 2007
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.21.5.a527
Subject(s) - connexin , gap junction , arteriogenesis , angiogenesis , anatomy , femoral artery , vascularity , gene expression , messenger rna , biology , ligation , medicine , andrology , endocrinology , pathology , microbiology and biotechnology , intracellular , gene , biochemistry
The vascular system remodels in response to mechanical stress. These responses may entail intercellular communication via gap junctions, composed of connexins. Little is known about connexin expression or gap junction communication in vessels undergoing angiogenesis or arteriogenesis. Using a mouse model of ischemia, femoral artery ligation, we hypothesized that connexin expression would be altered with vascular remodeling. In 6 female mice (age=22–39 wk), the femoral artery was removed between the inguinal ligament and popliteal bifurcation. A sham surgery was performed on the opposite leg. The animals recovered for 3 days, were anesthetized, and adductor, soleus, and gastrocnemius muscles were removed. RNA was isolated from each muscle sample, and mRNA expression was quantified for connexins (Cx37, Cx40, Cx43), eNOS, and the angiogenic marker PlGF in all muscles, and the longevity gene SIRT1 in the gastrocnemius, using real‐time RT‐PCR. Genes were standardized to smooth muscle alpha actin mRNA (to control for vascularity), beta‐actin mRNA, and total RNA. There were no significant differences (p<0.05) in the connexins, eNOS, PlGF, or SIRT1 in any of the muscles examined in the experimental leg compared to the sham leg, suggesting that gap junctions are stable during early angiogenesis, and that gap junctional communication is sustained in an ischemic model. Supported by NHLBI and HHMI‐UBSEP.