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Aging impairs mouse skeletal muscle macrophage polarization and muscle-specific abundance during recovery from disuse.

08:00 EDT 9th April 2019 | BioPortfolio

Summary of "Aging impairs mouse skeletal muscle macrophage polarization and muscle-specific abundance during recovery from disuse."

Impaired recovery of aged muscle following a disuse event is unresolved issue facing the older adult population. Although investigations in young animals has suggested that rapid regrowth of skeletal muscle following a disuse event involves a coordinated involvement of skeletal muscle macrophages, this phenomenon has not yet been thoroughly tested as an explaination for impaired muscle recovery in aging. To examine this hypothesis, young (3 month) and old (24-26 month) malemice were examined as controls, following 2 weeks of hindlimb unloading (HU) and following 4 (RL4)and 7 (RL7)days of reloading after HU. Muscles were harvested to assess muscle weight, myofiber-specifc cross-sectional area, and skeletal muscle macrophages via IF. Flow cytometry was used on gastrocnemius and soleus (at RL4)single cell suspensions to immunophenotype skeletal muscle macrophages. Our data demonstrated an impaired muscle regrowth in aged compared to young mice following disuse, which is characterized by divergent muscle macrophage polarization patterns and muscle-specifc macrophage abundance. During reloading, young mice exhibited the classical increase in M1-like (MHC IICD206) macrophages that preceeded the increase in percentage of M2-like macrophages (MHC IICD206), however old mice did not demonstrate this pattern. Also, at RL4, the soleus demonstrated reduced macrophage abundance with aging. Together, these data suggest that dysregulated macrophage phenotype patterns in aged muscle during recovery from disuse may be related to impaired muscle growth. Further investigation is needed to determine if the dysregulated macrophage response in the old during regrowth from disuse is related to a reduced ability to recruit or activate specific immune cells.

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This article was published in the following journal.

Name: American journal of physiology. Endocrinology and metabolism
ISSN: 1522-1555
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