Mitochondrial Biogenesis is Dysregulated in Thyroid Hormone Depleted Muscle Cells Despite Stimulatory Effects of Formoterol

Date
2020
Authors
Zumbro, Emily L.
Guerin, Gena D.
Gordon, Ryan A.
White, Chase M.
McAdams, Dreanna M.
Sokoloski, Matthew L.
Nichols, David L., Ph. D.
Duplanty, Anthony A.
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Abstract

Skeletal muscle (SKM) is an important regulator of metabolism with thyroid hormone (TH) being an important factor in mitochondrial biogenesis. PURPOSE: The purpose of this study was to explore mitochondrial dysregulation in a hypothyroid In Vitro model and examine the influence of an exercise mimetic, formoterol, on this pathway. METHODS: SKM myoblasts were TH depleted (ThD), ThD plus formoterol stimulation (ThD+F), or control cells (CON) with total RNA extracted during mid-myogenesis (D4) and at terminal differentiation (D6). Gene expression for PGC-1α, TFAM, and NRF1 was analyzed by qPCR. RESULTS: ThD media resulted in reduced NRF1 and TFAM. ThD+F resulted in increased PGC-1α (regulator of mitochondrial biogenesis) but decreased expression of its downstream targets TFAM and NRF1. CONCLUSION: Formoterol increases initial stimulation of mitochondrial biogenesis (PGC-1α) but related downstream signaling is decreased by TH depletion (TFAM and NRF1). This suggests that overall exercise signaling may be impaired by Hypothyroidism.

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Creative Arts and Research Symposium
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