Effect Of Oxidative Stress-Induced Endothelial Dysfunction On Myoblast Proliferation

Age-related skeletal muscle dysfunction is a major health concern for older adults, increasing the risk of hospitalization, mortality, and costs. Endothelial dysfunction has been suggested to contribute to sarcopenia. The age-associated decline in endothelial function is partly due to elevated reactive oxygen species (ROS) levels. In addition to the delivery/removal functions of the skeletal muscle microvasculature, the proximity of skeletal muscle and endothelial cells facilitates cell-to-cell communication. PURPOSE: To investigate if oxidative stress-induced endothelial dysfunction impairs primary human skeletal muscle satellite cell (hMuSC) proliferation through cell-to-cell communication. METHODS: Human umbilical vein endothelial cells (HUVECs) were exposed to 50 μM H2O2 for 48 hr, and cellular ROS was measured after removal of H2O2 media. Media was collected from Control (CON) and H2O2 treated cells for use on hMuSC. hMuSC were grown in a 50/50 mixture of skeletal muscle growth media and HUVEC CON or H2O2 media for 6 days. HUVEC oxidative stress was measured by ROS levels (n = 8). hMuSC proliferation was measured by EdU (n = 2). Data are Mean + SD. RESULTS: H2O2 treatment increased HUVEC ROS levels (Fig A). hMuSC incubated in oxidatively stressed HUVEC media (H2O2) lowered proliferation by ~20% (not statistically significant) compared to CON (Fig B). CONCLUSION: These preliminary results suggest that H2O2 induced oxidative stress in ECs might impair hMuSC proliferation. This research project was supported by an American Heart Association (AHA) grant 20IPA35360013.This research project was supported by an American Heart Association (AHA) grant 20IPA35360013.