Lactate induces C2C12 myoblasts differentiation by mediating ROS/p38 MAPK signalling pathway

Area of Science:

• Muscle Biology
• Cell Signaling
• Biochemistry

Background:

• Lactate is recognized as an energy substrate for skeletal muscle.
• Emerging evidence suggests lactate's regulatory role in myogenic differentiation.
• Lactate influences reactive oxygen species (ROS) levels during muscle cell processes.

Purpose of the Study:

• To investigate the effects of lactate on C2C12 myoblast differentiation.
• To elucidate the roles of ROS and p38 MAPK signaling in lactate-mediated myogenesis.
• To understand the interplay between lactate, ROS, and p38 MAPK in skeletal muscle differentiation.

Main Methods:

• Utilized C2C12 myoblasts for in vitro differentiation studies.
• Administered lactate at physiological concentrations to assess its impact.
• Employed n-acetylcysteine (NAC) as a ROS scavenger and SB203580 as a p38 MAPK inhibitor.
• Monitored myogenic differentiation markers (Myf5, MyoD, MyoG) and p38 MAPK phosphorylation.

Main Results:

• Lactate significantly enhanced C2C12 myoblast differentiation in a dose-dependent manner.
• Lactate-induced differentiation was accompanied by increased ROS production.
• NAC pretreatment attenuated lactate's effect on differentiation and p38 MAPK phosphorylation.
• SB203580 pretreatment inhibited lactate-induced C2C12 myoblast differentiation.
• Lactate-induced ROS generation was found to mediate p38 MAPK activation.

Conclusions:

• Lactate promotes C2C12 myoblast differentiation through a ROS-dependent mechanism.
• The p38 MAPK signaling pathway is crucial for lactate-mediated myogenesis.
• Lactate's beneficial role in myogenesis involves ROS-sensitive pathways.
• Findings suggest a positive impact of ROS in skeletal muscle function via lactate signaling.