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Vannathirai Book Hot Stills
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FilmiChakkar’s Forum. Hot Stills Gallery. Home » Site » Vannathirai. Aarman, Anand, Arjun, Badrinath, Bobby Simha, Damodar, Dilip Kumar, Disha, Govindarajan, Kasaragod, Krishnamoorthy, Muthusamy, Nasser, Nithiyanandan, Pradeep, Shri Krishna, Shyam, T Devyani.The objective of this proposal is to investigate the hypothesis that both the prolonged up-regulation of the glucocorticoid receptor (GR) and increased GR levels that appear in various stress-induced, neuroendocrine-related diseases are in large part, a direct result of the activation of the HPA axis during chronic stress. In our previous studies we determined that up-regulation of GR in some disease states was a direct consequence of activation of the HPA axis. We have now demonstrated that GR levels, and GR expression are also increased during the chronic stress condition. Our clinical data are consistent with the hypothesis that HPA hyperactivity results in prolonged up-regulation of GRs. We will be addressing this hypothesis in three Specific Aims. First, we will characterize the biological mechanisms responsible for GR up-regulation in order to define any direct GR regulation by hormones in the chronically stressed state. The mechanism by which the HPA axis is activated during chronic stress will be assessed. We will investigate whether all the hormones that are implicated in the stress response regulate GRs. We will compare GR mRNA and protein levels in the hypothalamic paraventricular nucleus (PVN) and hippocampus. Finally, we will investigate whether GR regulation occurs in human brain tumors, and whether a correlation exists between GR regulation and the activation of the HPA axis. Specific Aim 2 will investigate the factors which are responsible for the maintenance of GR expression in stress-induced diseases. Two lines of research are proposed: (a) to examine whether stress-induced increases in GR levels are due to an up-regulation of GR levels or a change in GR stability and (b) to investigate whether GRs are targeted for proteasomal degradation, thus rendering the receptor less responsive to hormone stimulation. Finally, Specific Aim 3 will investigate the GR-regulated molecular events and identify protein factors which may modulate GR levels in human brain tumors
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