Effects of transforming growth factor-beta (TGF-β1) on satellite cell activation and survival during oxidative stress

Abstract

The regulation of adult skeletal muscle repair and regeneration is largely due to the contribution of resident adult myogenic precursor cells called satellite cells. The events preceding their participation in muscle repair include activation (exit from quiescence), proliferation, and differentiation. This study examined the effects of transforming growth factor-beta (TGF-β1) on satellite cell activation, determined whether TGF-β1 could maintain quiescence in the presence of hepatocyte growth factor (HGF), and whether the regulation of satellite cell activation with TGF-β1 improves the ability of satellite cells to withstand oxidative stress. The addition of TGF-β1 during early satellite cell activation (0-48 h) or during the proliferative phase (48-96 h) maintained and induced satellite cell quiescence, respectively, as determined by myogenic differentiation (MyoD) protein expression. TGF-β1 also attenuated satellite cell activation when used with HGF. Finally, the role of quiescence in protecting cells against oxidative stress was examined. TGF-β1 treatment and the low pH satellite cell preparation procedure, a technique that forestalls spontaneous activation in vitro, both enhanced survival of cultured satellite cells following hydrogen peroxide treatment. These findings indicate that TGF-β1 is capable of maintaining and inducing satellite cell quiescence and suggest methods to maintain satellite cell quiescence may improve their transplantation efficiency.

Evaluation of muscle regeneration in aged animals after treatment with low-level laser therapy

“…However, this cytokine also has an influence on the state of satellite cell quiescence, as verified by Rathbone et al 27 . The addition of TGF-β1 in the first 48 hours of the satellite cell culture of adult rats provided a reduction in the quantity of MyoD, demonstrating that TGF-β1 interferes with cell activation, causing the cells to remain in a state of quiescence.…”

Factors secreted from high glucose treated endothelial cells impair expansion and differentiation of human skeletal muscle satellite cells

“…Oxidative and inflammatory environments decrease SC proliferation (Degens, ; Rathbone et al . ; Sente et al . ) as a result of downregulation of cyclin D1 and cell cycle arrest (Pyo et al .…”

“…Although these factors did not initiate an inflammatory response in satellite cells, they may have contributed to altered cell cycle regulation. Oxidative and inflammatory environments decrease SC proliferation (Degens, 2010;Rathbone et al 2011;Sente et al 2016) as a result of downregulation of cyclin D1 and cell cycle arrest (Pyo et al 2013). In vivo, conditions marked by chronic inflammation and endothelial dysfunction (ageing, diabetes) display decreases in total satellite cell number and an impaired ability to properly maintain and replenish the satellite cell pool (Gibson & Schultz, 1983;Day et al 2010;…”

The Potential of Combination Therapeutics for More Complete Repair of Volumetric Muscle Loss Injuries: The Role of Exogenous Growth Factors and/or Progenitor Cells in Implantable Skeletal Muscle Tissue Engineering Technologies

“…Influence quiescent SC activation and migration to the site of injury [Tatsumi et al, 1998] Induce proliferation of endothelial and smooth muscle cells and facilitate angiogenesis [Xin et al, 2001] FGF Promote SC activation and proliferation [Han et al, 2012] Promote endothelial cell proliferation and migration [Oladipupo et al, 2014] Promote neurogenesis [Kang and Hebert, 2015] IGF Simultaneously stimulate myoblast proliferation, differentiation, and myotube formation [Charge and Rudnicki, 2004;Gardner et al, 2015;Retamales et al, 2015] Influence nerve growth and contribute to decreased fibrosis and inflammation [Caroni and Grandes, 1990;Pelosi et al, 2007;Philippou and Barton, 2014] VEGF Promote SC activation and proliferation, as well as myoblast migration and survival [Arsic et al, 2004;Montarras et al, 2013] Promote endothelial cell migration and proliferation, and stimulate production of matrix metalloproteinases [Ferrara, 2002] Provide neuroprotective properties influencing tissue reinnervation after injury [Llado et al, 2013;Shvartsman et al, 2014] TGF Downregulate myogenesis by inducing SC quiescence and inhibiting proliferation and differentiation [Li et al, 2009;Rathbone et al, 2011] Influence ECM deposition and reorganization, and regulate motoneuron survival NGF Regulate the differentiation, survival, and maintenance of neurons [Micera et al, 2007] Enhance the fusogenic potential of myoblasts and enable reinnervation and angiogenesis of newly formed muscle [Chevrel et al, 2006;Deponti et al, 2009;Karatzas et al, 2013] Components for VML Restoration present, direct comparisons and conclusions on overall utility of growth factor-based applications among the various studies are not yet possible due to variations not only in the materials employed, but also in the combinations of different growth factors that were applied, as well as differences in the concentrations utilized. In addition, there are still no standardized descriptions of methods, procedures, and evaluation metrics for assessing the comparative efficacy of these treatments (i.e., the degree of functional recovery) [Miller et al, 2000;Hill et al, 2006a, b;Stratos et ...…”