Characterizing mitochondrial phenotypes and MERCS in aged human skeletal muscle myoblasts

Area of Science:

• Cellular Biology
• Aging Research
• Mitochondrial Biology

Background:

• Skeletal muscle aging is associated with cellular senescence and mitochondrial dysfunction.
• Mitochondrial characteristics in aged human myoblasts are not well understood.
• Cellular senescence involves complex molecular and morphological changes.

Purpose of the Study:

• To characterize mitochondrial function, morphology, and mitochondria-ER contacts in aged human myoblasts.
• To investigate the relationship between cellular senescence, oxidative stress, and mitochondrial alterations in aging muscle.
• To explore the role of mitochondria-endoplasmic reticulum contact sites (MERCS) in cellular aging.

Main Methods:

• Primary skeletal muscle myoblasts from young and elderly donors were analyzed.
• Assessed senescence markers (SA-β-gal, Lamin B1).
• Evaluated mitochondrial function (oxygen consumption, membrane potential), morphology, DNA content, and MERCS.

Main Results:

• Aged myoblasts displayed senescence markers and increased mitochondrial oxidative stress.
• Mitochondria showed hyperfusion and increased DNA content in aged cells.
• MERCS were elevated in aged myoblasts and correlated with mitochondrial oxidative stress.

Conclusions:

• Cellular aging in human myoblasts involves mitochondrial hyperfusion and increased MERCS.
• Elevated MERCS may be linked to mitochondrial oxidative stress.
• These adaptations might help maintain mitochondrial function during aging under stress.