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Direct conversion of human myoblasts into brown‐like adipocytes by engineered super‐active PPARγ
Author(s) -
Zhu Yanbei,
Yang Rongze,
McLenithan John,
Yu Daozhan,
Wang Hong,
Wang Yaping,
Singh Devinder,
Olson John,
Sztalryd Carole,
Zhu Dalong,
Gong DaWei
Publication year - 2015
Publication title -
obesity
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.438
H-Index - 199
eISSN - 1930-739X
pISSN - 1930-7381
DOI - 10.1002/oby.21062
Subject(s) - peroxisome proliferator activated receptor , chemistry , myocyte , microbiology and biotechnology , peroxisome , cancer research , medicine , biology , biochemistry , receptor
Objective To determine whether super‐activation of PPARγ can reprogram human myoblasts into brown‐like adipocytes and to establish a new cell model for browning research. Methods To enhance the PPARγ signaling, M3, the transactivation domain of MyoD, was fused to PPARγ. PPARγ and M3‐PPARγ‐lentiviral vectors were used to convert human myoblasts into adipocytes. Brown adipocyte markers of the reprogrammed adipocytes were assessed by qPCR and protein analyses. White adipocytes differentiated from subcutaneous stromal vascular cells and perithyroid brown fat tissues were used as references. Results In transient transfections, M3‐PPARγ had a stronger constitutive activity than PPARγ by reporter assay. Although the transduction of either PPARγ or M3‐PPARγ induced adipogenesis in myoblasts, M3‐PPARγ drastically induced the brown adipocyte markers of UCP1, CIDEA, and PRDM16 by 1,050‐, 2.4‐, and 5.0‐fold, respectively, and increased mitochondria contents by 4‐fold, compared to PPARγ. Conclusions Super‐activation of PPARγ can effectively convert human myoblasts into brown‐like adipocytes and provide a new approach to derive brown‐like adipocytes.