Up‐regulation of uncoupling protein 3 by thyroid hormone, peroxisome proliferator‐activated receptor ligands and 9‐cis retinoic acid in L6 myotubes

FEBS Letters

Nagase, Itsuro¹  Saito, Masayuki¹  Yoshida, Toshihide³  Kimura, Kazuhiro¹  Canas, Xavier¹  Irie, Yukiko¹  Yoshida, Shigeru² 

[1] Department of Biomedical Sciences, Laboratory of Biochemistry, Graduate School of Veterinary Medicine, Hokkaido University, Sapporo 060-0818, Japan;Pharmacology Laboratories, Institute for Drug Discovery Research, Yamanouchi Pharmaceutical Co., Ltd., Tsukuba 305-8566, Japan;First Department of Internal Medicine, Kyoto Prefectural University of Medicine, Kyoto 602-8566, Japan

关键词: Uncoupling protein 3;    L6 myotube;    PPAR;    Fatty acid;    T3;    Retinoic acid;   

DOI  :  10.1016/S0014-5793(99)01477-5

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

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.

【 授权许可】

Unknown