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BMP4 and BMP7 induce the white-to-brown transition of primary human adipose stem cells.
Am. J. Physiol.-Cell Physiol. 306, C431-C440 (2014)
While white adipose tissue (AT) is an energy storage depot, brown AT is specialized in energy dissipation. Uncoupling protein 1 (UCP1)-expressing adipocytes with a different origin than classical brown adipocytes have been found in white AT. These "brite" (brown-in-white) adipocytes may represent a therapeutic target to counteract obesity. Bone morphogenetic proteins (BMPs) play a role in the regulation of adipogenesis. Based on studies with murine cells, BMP4 is assumed to induce stem cell commitment to the white adipocyte lineage, whereas BMP7 promotes brown adipogenesis. There is evidence for discrepancies between mouse and human AT. Therefore, we compared the effect of BMP4 and BMP7 on white-to-brown transition in primary human adipose stem cells (hASCs) from subcutaneous AT. Long-term exposure of hASCs to recombinant BMP4 or BMP7 during differentiation increased adipogenesis, as determined by lipid accumulation and peroxisome proliferator-activated receptor-γ (PPARγ) expression. Not only BMP7, but also BMP4, increased UCP1 expression in hASCs and decreased expression of the white-specific marker TCF21. The ability of hASCs to induce UCP1 in response to BMP4 and BMP7 markedly differed between donors and could be related to the expression of the brite marker CD137. However, mitochondrial content and oxygen consumption were not increased in hASCs challenged with BMP4 and BMP7. In conclusion, we showed for the first time that BMP4 has similar effects on white-to-brown transition as BMP7 in our human cell model. Thus the roles of BMP4 and BMP7 in adipogenesis cannot always be extrapolated from murine to human cell models.
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Anmerkungen
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Publikationstyp
Artikel: Journalartikel
Dokumenttyp
Wissenschaftlicher Artikel
Schlagwörter
Adipogenesis ; Bone Morphogenetic Proteins ; Brite Adipocytes ; Primary Human Preadipocytes
Sprache
englisch
Veröffentlichungsjahr
2014
HGF-Berichtsjahr
0
ISSN (print) / ISBN
0363-6143
e-ISSN
1522-1563
Zeitschrift
American Journal of Physiology - Cell Physiology
Quellenangaben
Band: 306,
Heft: 5,
Seiten: C431-C440
Verlag
American Physiological Society
Begutachtungsstatus
Peer reviewed
Institut(e)
German Center for Diabetes Reseach (DZD)
PubMed ID
24284793
Erfassungsdatum
2014-12-31