Combined hypoxia hypercapnia delays apoptosis and maintains CD34 cell surface antigen

This paper examines the interactive effect of varying the concentrations of O2 (1, 5, 20 %) and CO2 (5, 15, 20 %) on human BM-derived promyeloblast (KG-1a) apoptosis, necrosis, proliferation, and CD34 maintenance. In short, the interactive effect of hypoxia (low levels of O2) and hypercapnia (high levels of CO2) showed increased CD34+ cell count and survival, and delayed apoptosis and necrosis, therefore maintaining cell identity and stemness while prolonging cell survival. This may suggest that maintaining cell identity and proliferation requires exposure of cells to both combined hypoxic and hypercapnic gas conditions in vivo, where the spatial distribution of the concentrations of these gases remains not well understood. We hypothesize that hypercapnia may counter -regulate activation of the mitochondrial apoptotic pathway by reducing intracellular pH, thus preventing the binding of anti-and pro-apoptotic proteins on the mitochondrial outer membrane (MOM). The interactive effect of hypoxia and hypercapnia may regulate several transcriptional factors such as hypoxia inducible factors (HIFs) and nuclear factor kappa-light-chain-enhancer of activated B-cells (NF-kappa B), thus facilitating delay in apoptosis and retaining of stem cell identity. Combined hypoxia and hypercapnia may play a key role in the prolonged survival of primitive hematopoietic stem cells (HSCs) in the stem cell niche of the bone marrow (BM). This study provides a potential foundation for enhancing proliferation systems of HSC while maintaining their stemness.

Automated summary

This study examines the effects of varying concentrations of oxygen and carbon dioxide on human bone marrow cells. The results suggest that low oxygen and high carbon dioxide conditions help maintain cell identity and stemness, and prolong cell survival. This study is important for enhancing stem cell proliferation systems while preserving their stemness.