NYMC Faculty Publications

Stress-Induced Changes in Gene Expression of Urocortin 2 and Other CRH Peptides in Rat Adrenal Medulla: Involvement of Glucocorticoids

Author Type(s)

Faculty

DOI

10.1111/jnc.12152

Journal Title

Journal of Neurochemistry

First Page

185

Last Page

192

Document Type

Article

Publication Date

4-1-2013

Department

Biochemistry and Molecular Biology

Keywords

Adrenal Medulla, Animals, Corticotropin-Releasing Hormone, Gene Expression Regulation, Glucocorticoids, Male, Mice, Knockout, Peptides, Rats, Rats, Sprague-Dawley, Real-Time Polymerase Chain Reaction, Receptors, Corticotropin-Releasing Hormone, Restraint, Physical, Stress, Psychological, Urocortins, CRF Receptor, Type 1

Disciplines

Medicine and Health Sciences

Abstract

The corticotropin-releasing hormone (CRH) family regulates the endocrine stress response. Here, we examined the effect of immobilization stress (IMO) on gene expression of adrenomedullary CRH family members. Urocortin 2 (Ucn2) has the highest basal gene expression and is increased by > 30-fold in response to single IMO and about 10-fold after six daily repeated IMO. IMO also induced a smaller rise in CRH (six-fold) and CRH receptor type 1 (CRHR1; two-fold with single IMO). The influence of glucocorticoids was examined. Dexamethasone (DEX) or corticosterone greatly increased Ucn2 mRNA levels in PC12 cells in a dose-dependent manner. The DEX elicited rise in Ucn2 was abolished by actinomycin D pre-treatment, indicating a transcriptionally mediated response. DEX also triggered a rise in CRHR1 and lowered CRH mRNA levels. In CRH-knockout mice, where the IMO-induced rise in corticosterone was attenuated, the response of IMO on Ucn2, as well as CRHR2 mRNAs was absent. Overall, the results suggest that the stress-triggered rise in glucocorticoids is involved in the large induction of Ucn2 mRNA levels by IMO, which may allow Ucn2 to act in an autocrine/paracrine fashion to modulate adrenomedullary function, or act as an endocrine hormone.

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