We at HypOxygen hope you had a constructive World Heart Day! The World Heart Federation prompts us to find ways to create a heart-healthy environment by exercising more and eating more healthily. Work by our HypOxystation users demonstrates the benefits of creating healthy environments for cell culture, by providing more physiological, low oxygen conditions that let cells breathe. The closed culture workstation controls oxygen, CO2, temperature and humidity throughout the duration of culture and manipulation, ensuring that ambient air does not compromise the physiology and growth of the cells. Cardiovascular researchers all around the world are culturing their cells at physioxia in the HypOxystation.
In his 2016 paper on post-MI remodeling, HypOxystation user Li et al. investigated the role of miR-7a/b in cardiomyocytes responding to oxidative stress/hypoxia. Similarly to the conditions during and after MI, miR-7a/b and their target molecules PARP-1 and Sp1 protect cardiomyocytes from apoptosis and reduce fibrosis in an oxygen-dependent manner. The authors postulate that hypoxia-induced injury to the heart can be mitigated by modified miRNA expression, helping to prevent heart failure. As with Li’s work, the results obtained by another HypOxystation user, Jim Uniacke at University of Guelph, show “the importance of oxygen as a cell culture parameter when making physiological inferences.”
Another group of HypOxystation users in Spain describe the upregulatory effect of hypoxia on matrix-degrading metalloproteinases and migration of vascular smooth muscle cells VSMC’s as atherosclerosis develops (Revuelta-Lopez et al., 2015). Importantly, the authors found opposite effects of hypoxia on signaling and regulatory pathways in murine and human VSMC’s, due to extremely different modulation of the LRP1-pPyk2-MMP-9 axis in these cells, demonstrating that mouse models are not necessarily suitable for mechanistic studies of human vascular disease. The HypOxystation with its controlled low oxygen environment enabled insights into ERK1,2 phosphorylation regulation, which “like that of MMP9 activation, differs in normoxic and hypoxic mVSMC, indicating that the modulation of this pathway strongly depends on O2 availability in mVSMC.”
