Expression of Rasd1 in mouse endocrine pituitary cells and its response to dexamethasone
| Autor: | Chad D. Foradori, Robert J. Kemppainen, Chen-Che Jeff Huang, Laci Mackay |
|---|---|
| Rok vydání: | 2021 |
| Předmět: |
Male
endocrine system medicine.medical_specialty Somatotropic cell Physiology Biology Gonadotropic cell Dexamethasone Article Prolactin cell Mice 03 medical and health sciences Behavioral Neuroscience 0302 clinical medicine Glucocorticoid receptor Pituitary Gland Anterior Thyrotropic cell Internal medicine polycyclic compounds medicine Animals Glucocorticoids Cellular localization Endocrine and Autonomic Systems Pars intermedia 030227 psychiatry Psychiatry and Mental health Neuropsychology and Physiological Psychology Endocrinology Pituitary Gland Corticotropic cell Stress Psychological hormones hormone substitutes and hormone antagonists 030217 neurology & neurosurgery |
| Zdroj: | Stress |
| ISSN: | 1607-8888 1025-3890 |
| Popis: | Dexamethasone-induced Ras-related protein 1 (Rasd1) is a member of the Ras superfamily of monomeric G proteins that have a regulatory function in signal transduction. Rasd1, also known as Dexras1 or AGS1, is rapidly induced by dexamethasone (Dex). While prior data indicates that Rasd1 is highly expressed in the pituitary and that the gene may function in regulation of corticotroph activity, its exact cellular localization in this tissue has not been delineated. Nor has it been determined which endocrine pituitary cell type(s) are responsive to Dex-induced expression of Rasd1. We hypothesized that Rasd1 is primarily localized in corticotrophs and furthermore, that its expression in these cells would be upregulated in response to exogenous Dex administration. Rasd1 expression in each pituitary cell type both under basal conditions and 1-hour post Dex treatment were examined in adult male mice. While a proportion of all endocrine pituitary cell types expressed Rasd1, a majority of corticotrophs and thyrotrophs expressed Rasd1 under basal condition. In vehicle treated animals, approximately 50-60% of corticotrophs and thyrotrophs cells expressed Rasd1 while the gene was detected in only 15-30% of lactotrophs, somatotrophs, and gonadotrophs. In Dex treated animals, Rasd1 expression was significantly increased in corticotrophs, somatotrophs, lactotrophs, and gonadotrophs but not thyrotrophs. In Dex treated animals, Rasd1 was detected in 80-95% of gonadotrophs and corticotrophs. In contrast, Dex treatment increased Rasd1 expression to a lesser extent (55-60%) in somatotrophs and lactotrophs. Corticotrophs of the pars intermedia, which lack glucocorticoid receptors, failed to display increased Rasd1 expression in Dex treated animals. Rasd1 is highly expressed in corticotrophs under basal conditions and is further increased after Dex treatment, further supporting its role in glucocorticoid negative feedback. In addition, the presence and Dex-induced expression of Rasd1 in endocrine pituitary cell types, other than corticotrophs, may implicate Rasd1 in novel pituitary functions. |
| Databáze: | OpenAIRE |
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