title: A comparative examination of cortisol effects on muscle myostatin and HSP90 gene expression in salmonids.
abstract: Cortisol, the primary corticosteroid in teleost fishes, is released in response to stressors to elicit local functions, however little is understood regarding muscle-specific responses to cortisol in these fishes. In mammals, glucocorticoids strongly regulate the muscle growth inhibitor, myostatin, via glucocorticoid response elements (GREs) leading to muscle atrophy. Bioinformatics methods suggest that this regulatory mechanism is conserved among vertebrates, however recent evidence suggests some fishes exhibit divergent regulation. Therefore, the aim of this study was to evaluate the conserved actions of cortisol on myostatin and hsp90 expression to determine if variations in cortisol interactions have emerged in salmonid species. Representative salmonids; Chinook salmon (Oncorhynchus tshawytscha), cutthroat trout (Oncorhynchus clarki), brook trout (Salvelinus fontinalis), and Atlantic salmon (Salmo salar); were injected intraperitoneally with a cortisol implant (50μg/g body weight) and muscle gene expression was quantified after 48h. Plasma glucose and cortisol levels were significantly elevated by cortisol in all species, demonstrating physiological effectiveness of the treatment. HSP90 mRNA levels were elevated by cortisol in brook trout, Chinook salmon, and Atlantic salmon, but were decreased in cutthroat trout. Myostatin mRNA levels were affected in a species, tissue (muscle type), and paralog specific manner. Cortisol treatment increased myostatin expression in brook trout (Salvelinus) and Atlantic salmon (Salmo), but not in Chinook salmon (Oncorhynchus) or cutthroat trout (Oncorhynchus). Interestingly, the VC alone increased myostatin mRNA expression in Chinook and Atlantic salmon, while the addition of cortisol blocked the response. Taken together, these results suggest that cortisol affects muscle-specific gene expression in species-specific manners, with unique Oncorhynchus-specific divergence observed, that are not predictive solely based upon mammalian stress responses.
authors.affiliation: Department of Biology, University of Alabama at Birmingham, Birmingham, AL 35294, USA.
authors.forename: Nicholas J
authors.initials: NJ
authors.lastname: Galt
authors.affiliation: USGS, Leetown Science Center, S.O. Conte Anadromous Fish Research Laboratory, Turners Falls, MA, USA.
authors.forename: Stephen D
authors.initials: SD
authors.lastname: McCormick
authors.affiliation: Department of Biology, University of Alabama at Birmingham, Birmingham, AL 35294, USA.
authors.forename: Jacob Michael
authors.initials: JM
authors.lastname: Froehlich
authors.affiliation: Department of Biology, University of Alabama at Birmingham, Birmingham, AL 35294, USA. Electronic address: pegbiga@uab.edu.
authors.forename: Peggy R
authors.initials: PR
authors.lastname: Biga
mesh_terms: D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D005260:Female; D005786:Gene Expression Regulation / Q000187:drug effects*; D018841:HSP90 Heat-Shock Proteins / Q000235:genetics* / Q000378:metabolism; D006854:Hydrocortisone / Q000008:administration & dosage / Q000097:blood / Q000494:pharmacology*; D008297:Male; D009132:Muscles / Q000187:drug effects / Q000378:metabolism*; D055435:Myostatin / Q000235:genetics* / Q000378:metabolism; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D012474:Salmon / Q000097:blood / Q000235:genetics*; D013045:Species Specificity
chemical_list: D001786:Blood Glucose; D018841:HSP90 Heat-Shock Proteins; D055435:Myostatin; D012333:RNA, Messenger; D006854:Hydrocortisone
keywords: Growth; HSP90; Hormone; Myostatin; Stress