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DIFFERENTIAL EXPRESSION OF MYOSTATIN AND ATROGIN-1 IN STRIATED MUSCLE EXPOSED TO HYPOXIA

Abstract

Hypoxia is characterized by an inadequate supply of oxygen to the body’s tissues occurring when traveling to or residing at high altitudes. The response to hypoxia is tissue-dependent, and in striated muscle (cardiac muscle -right and left ventricles and skeletal muscle), hypoxia exposure results in different hypertrophic and atrophic responses that are striated muscle dependent. In response to hypoxia, the right ventricle (RV) undergoes hypertrophy, the left ventricle (LV) remains mass stable, and the skeletal muscle (SkM) undergoes atrophy. PURPOSE: To determine mechanisms of differential hypertrophy/atrophy in the RV, LV, and SkM in response to acute and chronic hypoxia. METHODS: Male and female C57BL6 mice were placed in a hypobaric hypoxia chamber (HH; 17,000’) for four weeks (chronic hypoxia), three days (acute hypoxia), or remained at ambient air (control; 7220’). Tissue samples from the RV, LV, and the hind limb muscle complex (SkM), were collected. Reverse transcription polymerase chain reaction (qRT-PCR) was used to measure expression of myostatin (MSTN), a negative regulator of hypertrophy, and atrogin-1, a regulator of muscle protein breakdown. RESULTS: The expression of MSTN in SkM and the LV were unchanged in acute or chronic hypoxia. MSTN expression in the RV was unchanged in acute hypoxia but was upregulated fourfold compared to control with chronic hypoxia (p<0.001). Atrogin-1 expression was unchanged across all three muscle types. CONCLUSIONS: Although we establish that changes in muscle mass are tissue dependent, the mechanisms remain unclear but may involve differential activation of MSTN. Understanding these changes may help treat hypoxic disease and translate to individuals living at or journeying to high altitude.

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