A differential gene expression study in hypobaric hypoxia

Abstract

Oxygen is of fundamental importance to most living organisms. The ability of oxygen to act as the terminal electron acceptor in the respiratory chain allows efficient energy generation by living organisms. With increasing altitude, the concentration of oxygen remains the same, but the atmospheric pressure decreases and with this the partial pressure of oxygen falls. It is known that, immediately upon arrival of a lowlander at high altitude (HA), a number of changes in physiological parameters occur which enable the body to function optimally in the low oxygen environment. Among the few forth-mentioned HA disorders among sojourners, acute mountain sickness (AMS) and high altitude pulmonary edema (HAPE) are the two most important disorders. HAPE occurs following exposure to hypobaric hypoxia in otherwise normal individuals. While some families and individuals are at risk, those with a long ancestry at HA have a lower risk. Moreover, individuals who have had HAPE are at a greater risk of repeat events. Such data support a strong genetic component to HAPE susceptibility. Hypoxia is a pervasive physiological stimulus that affects all living organisms in unique ways, depending on their intrinsic cellular macromolecular constituents and their reaction products. The cellular responses to hypoxia are complex and characterized by alteration in the expression of a number of genes, including stress-related genes and corresponding proteins that are necessary to maintain homeostasis. A broader understanding of hypoxia induced alterations in cellular or organ function could be better achieved from the concerted application of functional genomics. The molecular details of hypoxia-induced cellular responses have not been fully explored. Hence it becomes necessary to study the differential gene expression under hypoxic conditions with the help of advanced techniques like microarray coupled with routinely used techniques like RT-PCR, western blot, real time PCR etc.