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Neuroprotection by estrogen under hypoglycemic condition with special emphasis on AKT_GSK pathway

Our previous studies have shown that estrogen is involved in the neuroprotection of cells under hypoglycemic conditions within 24 hrs. The hypothalamic cells (N38) were treated under various conditions (T1‐ media with 5%FBS and 1% Pen‐Strep at 24 hrs, T2‐ T1without glucose at 24 hrs, T3‐ T1 without glucose with 100 micro M estrogen, T4‐ T1 at 72 hrs, T5‐ T2 at 72hrs, T6‐ T3 at 72 hrs.). One of the possible pathway through which estrogen exerts its protection is through Akt‐GSK coupling. Akt regulates cell survival by phosphorylating components of cell death apparatus like glycogen synthase kinase‐3 (GSK3b). When the activity of AKT is at its highest, GSK3b is in its inhibited state leading to cell survival and vice versa. DNA microarray studies showed that AKT was down‐regulated and glycogen synthase upregulated in the absence of glucose and in the presence of estrogen there was an increase and decrease respectively in gene expression. Network/functional analysis gave further information of other signaling molecules upregulated by the estrogen treatment after hypoglycemic shock like MMP3, POSTN, LOX, PENK, TGFB1 at 72 hours whereas within 24 hours neurotrophin, NGF, KLK2, IF144 were upregulated and VMA21 downregulated. There were 11 genes that showed 1.5 fold change and 1 gene showing 2 fold change. Between T5 vs. T6 there were 58 genes that showed 1.5 and 3 genes showed above 2 fold change. The study raises the possibility of novel pharmacological interventions against hypoglycemia and use of estrogen against the neuronal deficits. The result supports ovarian steroid as modulators in CNS responsiveness to recurring glucoprivation and its mechanism of action through membrane receptors.