Reduced Gja5 expression in arterial endothelial cells impairs arteriogenesis during acute ischemic cardiovascular disease.

The aim of the present study was to investigate the functional role of gap junction protein α 5 (Gja5) in arterial endothelial cells in the arteriogenesis that occurs during acute ischemic cardiovascular disease. Gja5 knockout mice and the femoral artery occlusion (FAO) model were used in the current study. Perfusions of both hindlimbs were obtained separately prior to FAO, immediately following FAO and 1, 3, 7, 14 and 21 days after FAO using a Laser Doppler Flow Imager. Genetic evidence concerning the gastrocnemicus (GC) muscle was collected by reverse transcription-quantitative polymerase chain reaction. There were significant reductions in the hindlimb perfusion of Gja5-/- mice compared with Gja5+/+ mice 1, 3, 7, 14 and 21 days following FAO. In Gja5+/- and in Gja5+/+ mice, the expression of Gja5 in the GC muscle was increased 4-fold in the ischemic hindlimb 3 days following FAO. Levels of Gja5 expression then returned to baseline values 7 days after FAO. The results of the present study demonstrated that arterial Gja5 expression serves a functional role in acute ischemic cardiovascular disease.