Expression of Estrogen Receptor α and β in Rat Astrocytes in Primary Culture: Effects of Hypoxia and Glucose Deprivation

Estrogen replacement therapy could play a role in the reduction of injury associated with cerebral ischemia in vivo, which could be, at least partially, a consequence of estrogen influence of glutamate buffering by astrocytes during hypoxia/ischemia. Estrogen exerts biological effects through interaction with its two receptors: estrogen receptor alpha (ERa) and estrogen receptor beta (ER beta), which are both expressed in astrocytes. This study explored effects of hypoxia and glucose deprivation (HGD), alone or followed by 1 h recovery, on ERa and ER beta expression in primary rat astrocyte cultures following 1 h exposure to: a) 5 % CO2 in air (control group-CG); b) 2 % O-2/5 % CO2 in N-2 with glucose deprivation (HGD group-HGDG); or c) the HGDG protocol followed by 1 h CG protocol (recovery group-RG). ERa mRNA expression decreased in HGDG. At the protein level, full-length ERa (67 kDa) and three ER alpha-immunoreactive protein bands (63, 60 and 52 kDa) were detected. A significant decrease in the 52 kDa band was seen in HGDG, while a significant decrease in expression of the full length ERa was seen in the RG. ER beta mRNA and protein expression (a 54 kDa single band) did not change. The observed decrease in ERa protein may limit estrogen-mediated signalling in astrocytes during hypoxia and recovery.