Myosin heavy chain mRNA and protein distribution in immobilized rat skeletal muscle are not affected by testosterone status

Authors: Harjola; Jänkälä; Härkönen

Source: Acta Physiologica, Volume 169, Number 4, August 2000 , pp. 277-282(6)

Publisher: Wiley-Blackwell

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Abstract:

The effects of testosterone treatment and gonadectomy on myosin heavy chain (MHC) messenger RNA (mRNA) and protein expression after 1 week’s immobilization were studied in male rat gastrocnemius muscle. In the testosterone-treated group silastic testosterone capsules were implanted subcutaneously before immobilization. The gonadectomized animals were castrated at 5 weeks of age. One group of eugonadal animals served as the immobilized control group, and another as the sedentary control group. Immobilization was performed at 9 weeks of age by bilateral hindlimb casting. The body and muscle masses, and the amount of type IIa MHC mRNA decreased significantly (P < 0.01) in the immobilized animals by ~30, 40 and 50%, respectively, regardless of the serum testosterone levels which ranged from 1.1 ± 0.4 to 59 ± 14 nmol L−1. In the immobilized testosterone-treated group the proportion of type IIx MHC mRNA increased to 14% of the total MHC mRNA (P=0.02, compared with control). The MHC protein distribution did not change significantly. There were no significant differences in any parameters between the three immobilized groups. In conclusion, neither the lack nor excess of testosterone significantly altered the changes caused by immobilization. Therefore, it seems that lack of mechanical loading is a far more important determinant of MHC expression than the male sex hormone status.

Keywords: SDS–PAGE; androgens; castration; disuse; gastrocnemius; hypogonadism; number of MHC mRNA molecules; quantitative reverse transcriptase-polymerase chain reaction

Document Type: Research Article

DOI: http://dx.doi.org/10.1046/j.1365-201x.2000.00739.x

Affiliations: Department of Clinical Chemistry, Helsinki University Central Hospital, Finland

Publication date: August 1, 2000

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