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Transforming growth factor-beta1 upregulates myostatin expression in mouse C2C12 myoblasts.
J Physiol Pharmacol. 2005 Jun; 56 Suppl 3:195-214.JP

Abstract

Myostatin (MSTN) and transforming growth factor-beta1 (TGF-beta1) belong to the same TGF-beta superfamily of proteins. They are involved in regulation of skeletal muscle growth and development as well as muscle catabolism. The aim of the present study was to investigate the relationship between MSTN and TGF-beta1 expression in proliferating and differentiating mouse C2C12 myoblasts cultured in normal and catabolic conditions and to evaluate the effect of exogenous TGF-beta1 as well as "knock down" of TGF-beta1 receptor type II on MSTN expression in proliferating and differentiating myogenic cells. The direct effect of TGF-beta1 on myostatin was also examined. Myostatin expression increased gradually with cell confluency in proliferating cultures, while the level of TGF-beta1, detected in the form of a 100 kDa small latent complex diminished. Myostatin expression was accompanied by a partial cell cycle arrest. Three forms of myostatin were found: a 52 kDa precursor, a 40 kDa latency associated propeptide, and a 26 kDa active peptide. A decrease in myostatin and TGF-beta1 levels was observed during the first three days of differentiation, which was subsequently followed by significant increase of their expression during next three to four days of differentiation. Catabolic state induced by dexamethasone significantly increased the level of all forms of myostatin as well as latent (100 kDa) and active (25 kDa) forms of TGF-beta1 in differentiating myoblasts in a dose dependent manner. Exogenous TGF-beta1 (2 ng/ml) significantly increased myostatin levels both in proliferating and differentiating C2C12 myoblasts, whereas silencing of the TGF-beta1 receptor II gene significantly lowered myostatin level in examined cells. The presented results indicate that TGF-beta1 may control myostatin-related regulation of myogenesis through up-regulation of myostatin, predominantly in the course of terminal differentiation and glucocorticoid-dependent catabolic stimulation.

Authors+Show Affiliations

Department of Physiological Sciences, Faculty of Veterinary Medicine, Warsaw Agricultural University, Warsaw, Poland.No affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

16077203

Citation

Budasz-Rwiderska, M, et al. "Transforming Growth Factor-beta1 Upregulates Myostatin Expression in Mouse C2C12 Myoblasts." Journal of Physiology and Pharmacology : an Official Journal of the Polish Physiological Society, vol. 56 Suppl 3, 2005, pp. 195-214.
Budasz-Rwiderska M, Jank M, Motyl T. Transforming growth factor-beta1 upregulates myostatin expression in mouse C2C12 myoblasts. J Physiol Pharmacol. 2005;56 Suppl 3:195-214.
Budasz-Rwiderska, M., Jank, M., & Motyl, T. (2005). Transforming growth factor-beta1 upregulates myostatin expression in mouse C2C12 myoblasts. Journal of Physiology and Pharmacology : an Official Journal of the Polish Physiological Society, 56 Suppl 3, 195-214.
Budasz-Rwiderska M, Jank M, Motyl T. Transforming Growth Factor-beta1 Upregulates Myostatin Expression in Mouse C2C12 Myoblasts. J Physiol Pharmacol. 2005;56 Suppl 3:195-214. PubMed PMID: 16077203.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Transforming growth factor-beta1 upregulates myostatin expression in mouse C2C12 myoblasts. AU - Budasz-Rwiderska,M, AU - Jank,M, AU - Motyl,T, PY - 2005/01/28/received PY - 2005/05/05/accepted PY - 2005/8/4/pubmed PY - 2007/12/7/medline PY - 2005/8/4/entrez SP - 195 EP - 214 JF - Journal of physiology and pharmacology : an official journal of the Polish Physiological Society JO - J Physiol Pharmacol VL - 56 Suppl 3 N2 - Myostatin (MSTN) and transforming growth factor-beta1 (TGF-beta1) belong to the same TGF-beta superfamily of proteins. They are involved in regulation of skeletal muscle growth and development as well as muscle catabolism. The aim of the present study was to investigate the relationship between MSTN and TGF-beta1 expression in proliferating and differentiating mouse C2C12 myoblasts cultured in normal and catabolic conditions and to evaluate the effect of exogenous TGF-beta1 as well as "knock down" of TGF-beta1 receptor type II on MSTN expression in proliferating and differentiating myogenic cells. The direct effect of TGF-beta1 on myostatin was also examined. Myostatin expression increased gradually with cell confluency in proliferating cultures, while the level of TGF-beta1, detected in the form of a 100 kDa small latent complex diminished. Myostatin expression was accompanied by a partial cell cycle arrest. Three forms of myostatin were found: a 52 kDa precursor, a 40 kDa latency associated propeptide, and a 26 kDa active peptide. A decrease in myostatin and TGF-beta1 levels was observed during the first three days of differentiation, which was subsequently followed by significant increase of their expression during next three to four days of differentiation. Catabolic state induced by dexamethasone significantly increased the level of all forms of myostatin as well as latent (100 kDa) and active (25 kDa) forms of TGF-beta1 in differentiating myoblasts in a dose dependent manner. Exogenous TGF-beta1 (2 ng/ml) significantly increased myostatin levels both in proliferating and differentiating C2C12 myoblasts, whereas silencing of the TGF-beta1 receptor II gene significantly lowered myostatin level in examined cells. The presented results indicate that TGF-beta1 may control myostatin-related regulation of myogenesis through up-regulation of myostatin, predominantly in the course of terminal differentiation and glucocorticoid-dependent catabolic stimulation. SN - 1899-1505 UR - https://www.unboundmedicine.com/medline/citation/16077203/Transforming_growth_factor_beta1_upregulates_myostatin_expression_in_mouse_C2C12_myoblasts_ L2 - http://www.jpp.krakow.pl/journal/archive/06_05/pdf/195_06_05_article.pdf DB - PRIME DP - Unbound Medicine ER -