| Classification |
Proteins |
Physiological function |
References |
| Proteins of energy metabolism including |
Glycolytic
enzymes |
Often referred as hypoxia-associated proteins (HAPs), these proteins include the glycolytic enzyme GAPDH and non-neuronal enolase unique to endothelial cells. Expression of these proteins helps in up regulated tolerance and adaptation to lack of oxygen. This may be one of the mechanisms to overcome the ischemic injury during hypoxia. Increased expression of heat shock proteins have been found in hypoxic condition. |
[27,73,74] |
| Stress related proteins |
Heat shock Proteins (HSPs) |
The enhanced synthesis and accumulation of several functionally and compartmentally distinct families of HSPs, such as HSP70, HSP90, HSP60, and HSP27 is one of the cellular mechanisms for protection against the stress induced by environmental cues. Inflammatory responses during hypoxia are due to over expression of these proteins. |
[75,12,76] |
| Membrane-bound proteins that include transporters and receptors |
Acid-base transporters, glucose transporter |
The influence of intermittent hypoxia exposure on the expression of acid-base transporters in the mouse central nervous system, especially in the cerebellum is the decreased expression of sodium/hydrogen exchanger (NHE) isoform 1 and sodium-bicarbonate co-transporter. Edema of CNS due to hypoxia is related to alteration in these proteins. |
[77-79] |
| Cytosolic proteins |
Antioxidants, signalling cascade proteins |
The expression of antioxidants and the proteins associated with signalling cascade is altered in hypoxia. The expression of nitric oxide synthase (NOS) endothelial (eNOS) and inducible (iNOS) forms is increased during hypoxic condition. Overexpression of NOS leads to vasodilation to minimise the effect of hypoxia. |
[80-82] |
