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Up‐regulation of uncoupling protein 3 by thyroid hormone, peroxisome proliferator‐activated receptor ligands and 9‐ cis retinoic acid in L6 myotubes
Author(s) -
Nagase Itsuro,
Yoshida Shigeru,
Canas Xavier,
Irie Yukiko,
Kimura Kazuhiro,
Yoshida Toshihide,
Saito Masayuki
Publication year - 1999
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(99)01477-5
Subject(s) - thyroid hormone receptor , retinoic acid , thyroid hormone receptor beta , peroxisome proliferator activated receptor , chemistry , hormone , retinoic acid receptor , receptor , myogenesis , endocrinology , peroxisome , medicine , thyroid , peroxisome proliferator , biochemistry , hormone receptor , biology , gene , cancer , breast cancer
Uncoupling protein 3 (UCP3), expressed abundantly in the skeletal muscle, is one of the carrier proteins dissipating the transmitochondrial electrochemical gradient as heat, and thereby has been implicated in the regulation of energy metabolism. We have investigated UCP3 mRNA expression in the widely used L6 myocyte cell line by Northern blot analysis. UCP3 mRNA was not detected in L6 myoblasts, but appeared after their differentiation to myotubes. The UCP3 mRNA level was increased when L6 myotubes were treated with increasing concentrations of triiodothyronine (T3), oleic acid, α‐bromopalmitate and carbacyclin, a non‐selective ligand of peroxisome proliferator‐activated receptors (PPARs), whereas it was not influenced when treated with selective ligands of PPARα (WY 14 643) and PPARγ (troglitazone). A ligand of retinoid X receptor (RXR), 9‐ cis retinoic acid, was also effective by itself and in combination with carbacyclin in stimulating UCP3 mRNA expression. The mRNA analysis of individual PPAR isoforms revealed that L6 cell expressed a significant level of PPARδ but undetectable levels of PPARα and PPARγ. These results suggest that UCP3 expression in myocytes is differentiation‐dependent and regulated by the T3 receptor, RXR and PPARδ.

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