Abstract
Mitochondria are subcellular organelles that involved in ATP synthesis, ROS generation, apoptosis and aging, etc. Their morphologies influence cellular activities. When the balance of mitochondrial fusion and fission is lost under the exposure of supra-physiologic cyclic stretches, reactive oxygen species (ROS) are released and cells apoptosis is prompted. In previous study, the changes of the mitochondrial morphology were observed in the bovine aortic endothelial cells (BAEC) under supra-physiologic cyclic stretches. However, the underlying mechanisms remain obscure. In this study, we examined the relationship between the supra-physiologic cyclic stretches and the alteration of the mitochondrial morphology in human aortic endothelial cells (HAECs). To visualize the changes of mitochondrial morphology, HAECs were stained with 1.0μM Mito Tracker Orange, and then pretreated with 10μM GdCl_3 to inhibit stretch-induce intracellular Ca^<2+> increase involved in mitochondrial fission. HAECs were subjected to supra-physiologic cyclic stretches (20% at 1 Hz) by using a stretch camber with a stepper motor for 1 hour and mitochondrial morphologies were time-lapse imaged every 12 min. In HAECs under 20% cyclic stretch, the average length of mitochondria decreased in comparison with that of the control cells (0%), in both the presence and absence of the inhibitor, GdCl_3. These results indicate that the supra-physiologic cyclic stretch causes mitochondrial fragmentation involved in apoptosis via the pathway which is different from stretch-induce intracellular Ca^<2+> increase in HAECs.
