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

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dc.contributor.authorZumbro, Emily L.
dc.contributor.authorGuerin, Gena D.
dc.contributor.authorGordon, Ryan A.
dc.contributor.authorWhite, Chase M.
dc.contributor.authorMcAdams, Dreanna M.
dc.contributor.authorSokoloski, Matthew L.
dc.contributor.authorNichols, David L., Ph. D.
dc.contributor.authorDuplanty, Anthony A.
dc.date.accessioned2020-09-18T18:06:28Z
dc.date.available2020-09-18T18:06:28Z
dc.date.issued2020
dc.descriptionCreative Arts and Research Symposiumen_US
dc.description.abstractSkeletal 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.en_US
dc.identifier.urihttps://hdl.handle.net/11274/12492
dc.language.isoen_USen_US
dc.titleMitochondrial Biogenesis is Dysregulated in Thyroid Hormone Depleted Muscle Cells Despite Stimulatory Effects of Formoterolen_US
dc.typePosteren_US

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Student Creative Arts and Research Symposium | 2020
Student Creative Arts and Research Symposium | 2020