Regulation of bovine satellite cell proliferation and differentiation by insulin and triiodothyronine

Citation
I. Cassar-malek et al., Regulation of bovine satellite cell proliferation and differentiation by insulin and triiodothyronine, DOM ANIM EN, 17(4), 1999, pp. 373-388
Citations number
49
Categorie Soggetti
Animal Sciences","Animal & Plant Sciences
Journal title
DOMESTIC ANIMAL ENDOCRINOLOGY
ISSN journal
07397240 → ACNP
Volume
17
Issue
4
Year of publication
1999
Pages
373 - 388
Database
ISI
SICI code
0739-7240(199911)17:4<373:ROBSCP>2.0.ZU;2-X
Abstract
Satellite cells activity contributes to postnatal muscle growth. Herein, we have studied the respective influence of insulin and triiodothyronine (T3) on the proliferation and differentiation of primary bovine satellite cells isolated from Semitendinosus muscle of Montebeliard steers. Under basal co nditions, satellite cells proliferated until the fifth day of culture, bega n to fuse into myotubes and expressed differentiation markers such as conne ctin, myogenin, and myosin heavy chain (MHC) isoforms. Insulin behaved as a n effective mitogen. Moreover, it promoted extensive myotube formation and enhanced differentiation as shown by an increase in the accumulation of dif ferentiation markers. Maximal differentiation occurred with insulin physiol ogical range concentrations. A delay in the stimulation of differentiation was registered with a high dose that promoted maximal proliferation. Conver sely, T3 decreased cell proliferation in a dose-dependent manner. In additi on, fusion and biochemical differentiation (accumulation of connectin, MyoD 1, myogenin, and myosin heavy chain isoforms) were also enhanced. Bovine sa tellite cells seemed to respond differentially to insulin and T3 for prolif eration. Interestingly, both hormones displayed a myogenic influence. Our o bservations suggest that both hormones could influence bovine satellite cel ls in vivo and contribute to the regulation of postnatal muscle growth. (C) 1999 Elsevier Science Inc. All rights reserved.