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Regulation of avian uncoupling protein (av-UCP) expression by cytokines and hormonal signals in quail myoblast cells

Author:
Ferver, Alison, Dridi, Sami
Source:
Comparative biochemistry and physiology 2020 v.248 pp. 110747
ISSN:
1095-6433
Subject:
brown adipose tissue, energy, gene expression regulation, heat production, hormonal regulation, interleukin-6, leptin, mammals, messenger RNA, mitochondria, models, muscles, myoblasts, myocytes, peroxisome proliferator-activated receptor alpha, peroxisome proliferator-activated receptor gamma, quails, reactive oxygen species, transcription (genetics), tumor necrosis factor-alpha
Abstract:
Uncoupling proteins (UCPs), members of the mitochondrial anion carrier family, play a pivotal role in thermogenesis, redox balance, reactive oxygen species and many other cellular processes. They were extensively studied in mammalian species and have been shown to be tightly regulated at transcriptional and translational levels by various environmental and hormonal factors. Such studies are very limited in avian species which represent a unique model because they lack brown adipose tissue and they contain only one UCP (av-UCP) predominantly expressed in the muscle. The present study aimed, therefore, to determine the effects of pro-inflammatory cytokines (IL-6 and TNFα) and energy homeostasis-related hormones (leptin and T3) on the expression of av-UCP and its related transcription factors in quail myoblast (QM7) cells.Leptin treatment for 24 h significantly down-regulated av-UCP, and up-regulated PGC-1α, PPARα, and PPARγ expression in QM7 cells. IL-6 and TNFα administration significantly up-regulated the expression of av-UCP, however T3 had a biphasic effects (up-regulation with low dose and down-regulation with high dose) on av-UCP mRNA levels (P < .05). TNFα significantly induced PPARα and PPARγ mRNA abundances, however T3 and IL-6 down-regulated PPARα expression (P < .05).Together, these data are the first to report cytokine and hormonal regulation of av-UCP in avian muscle cells, suggesting that these effects are mediated through PPARs and PGC-1α, and opening a new vista for future functional and mechanistic studies.
Agid:
6997879