Percutaneous electrical stimulation-induced muscle contraction prevents the decrease in ribosome RNA and ribosome...

Area of Science:

• Muscle physiology and cellular biology
• Biomedical engineering and rehabilitation

Background:

• Skeletal muscle atrophy results from unloading, impacting ribosome synthesis and translational capacity.
• Ribosome synthesis is a key regulator of skeletal muscle mass.
• Percutaneous electrical muscle stimulation (pEMS) is used clinically to enhance muscle mass, but its effect on ribosome synthesis during unloading is unknown.

Purpose of the Study:

• To investigate the impact of daily pEMS on ribosome synthesis and content during mouse hindlimb unloading.
• To determine if pEMS can rescue the reduction in ribosome synthesis caused by muscle unloading.
• To elucidate the mechanisms by which pEMS may attenuate muscle atrophy.

Main Methods:

• Utilized a mouse model of hindlimb unloading (HU) via pelvic suspension.
• Administered daily pEMS to the gastrocnemius muscle in a subset of HU mice.
• Quantified ribosome synthesis markers (28S rRNA, rpL10, rpS3) and related proteins (phospho-p70S6K, UBF, Nufip1, LC3).

Main Results:

• Hindlimb unloading significantly reduced 28S rRNA, rpL10, and rpS3 expression.
• Daily pEMS treatment rescued these reductions in ribosome synthesis markers.
• pEMS increased phospho-p70S6K and UBF protein expression, suggesting enhanced synthesis pathways.
• pEMS attenuated the HU-induced increase in the autophagy marker LC3-II, indicating reduced ribosome degradation.

Conclusions:

• Daily pEMS treatment effectively prevents the reduction in ribosome synthesis and content during muscle unloading.
• pEMS may attenuate muscle atrophy by preserving ribosome synthesis and potentially reducing ribosome degradation.
• These findings offer insights into the mechanisms of pEMS in combating disuse-induced muscle atrophy.