Daily Spontaneous Running (Dsr) Decreases Phosphorylation Of Left Ventricular (Lv) Connexin-43 (Cx43) At Pathological Sites In Female Sprague-Dawley Rats

Cx43 is a gap junction expressed primarily in the LV of the heart that ensures efficient cell to cell communication. Down‐regulation of gap junctions often correlates with a pathological cardiovascular state, including ischemia and increased arrhythmogenesis. Regulation of Cx43 protein by post‐translational modification can enhance or down‐regulate gap junction assembly and function. Cardiovascular conditioning via exercise training has been well documented to prevent the incidence of arrhythmias. The goal of this study was to determine if DSR resulted in altered LV‐Cx43 expression and/or phosphorylation status. We hypothesized that cardiovascular conditioning with exercise training would elicit a reduced phosphorylation at sites known to decrease Cx43 function (S255, S262, S279/282, and S368). To simulate a conditioned state, rats underwent 9 weeks of DSR (n=4), compared to cage controls (n=4). Subsequently, Western blot analysis was performed to measure total and phosphorylated forms of Cx43 from the LV. Data indicate no change in Cx43 expression. However, the phosphorylation status was altered by DSR, with the greatest impact on S368. Specifically, there was a significant decrease in hyperphosphorylated Cx43‐pS368. Thus, cardiovascular conditioning with exercise may alter Cx43 phosphorylation status in a manner consistent with a cardioprotective effect against arrhythmogenesis. IOER‐3726.