Palmitate exerts opposite effects on proliferation and differentiation of skeletal myoblasts.

The purpose of the study was to examine mechanisms controlling cell cycle progression/arrest and differentiation of mouse C2C12 myoblasts exposed to long-chain saturated fatty acid salt, palmitate. Treatment of proliferating myoblasts with palmitate (0.1 mmol/l) markedly decreased myoblast number.

Insulin-Like Growth Factor-I Increases Laminin, Integrin Subunits and Metalloprotease ADAM12 in Mouse Myoblasts.

The extracellular matrix (ECM) is considered a part of the myogenesis signaling mechanism. we hypothesized that insulin-like growth factor-I (IGF-I) modifies ECM during differentiation of mouse C2C12 cells. The myogenic effect of IGF-I (30 nmol/l) was manifested by increased myogenin and myosin heavy chain (MyHC) levels as well as fusion index (2.

Transcriptional regulation of important cellular processes in skeletal myogenesis through interferon-γ.

The purpose of the present study was to investigate the effect of interferon (IFN)-γ on the transcriptomic profile of differentiating mouse C2C12 myogenic cells. Global gene expression was evaluated using whole mouse genome oligonucleotide microarrays, and the results were validated through real-time PCR. IFN-γ (1 ng/mL) increased myoblast proliferation but decreased cell respiration and myosin heavy chain content and slightly decreased the fusion index in differentiating C2C12 cell cultures.

[Interactions of proliferation and differentiation signaling pathways in myogenesis].

The commitment of myogenic cells in skeletal muscle differentiation requires earlier irreversible interruption of the cell cycle. At the molecular level, several key regulators of the cell cycle have been identified: cyclin-dependent kinases and their cyclins stimulate the cell cycle progress and its arrest is determined by the activity of cdk inhibitors (Cip/Kip and INK protein families) and pocket protein family: Rb, p107 and p130. The biological activity of cyclin/cdk complexes allows the successive phases of the cell cycle to occur.

[Systemic and local mechanisms leading to cachexia in cancer].

Cachexia is a multifactorial syndrome of atrophy of skeletal muscle and adipose tissue, resulting in progressive loss of body weight associated with low quality of life and poor prognosis in cancer. Studies on experimental animal models and observations on patients have shown that the soluble factors secreted by tumor cells and tissues of the patient can participate in regulation of the wasting process. Cachexia is often accompanied by anorexia, which is caused by predominance of signals inhibiting appetite in the hypothalamus, such as release of proopiomelanocortin and anorexigenic action of proinflammatory cytokines (IL-1α, IL-1β, IL-6, TNF-α).

[Maternal obesity and the development of skeletal muscle in offspring--fetal origin of metabolic disorders].

Suboptimal fetal environments due to inadequate maternal nutrition, obesity, inflammation or gestational diabetes expose the fetus to humoral cues that alter metabolism and growth parameters leading to metabolic disturbances later in life. The fetal stage is crucial for the development of skeletal muscle, a tissue playing an important role in metabolism. Maternal obesity induces inflammation in the fetus causing modifications in the development of fetal skeletal muscle.