期刊
PLOS ONE
卷 7, 期 9, 页码 -出版社
PUBLIC LIBRARY SCIENCE
DOI: 10.1371/journal.pone.0045352
关键词
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资金
- Sigrid Juselius Foundation
- Finnish Foundation for Cardiovascular Research
- Magnus Ehrnrooth Foundation
- Liv och Halsa Foundation
- Novo Nordisk Foundation
- Academy of Finland [121457]
- EU FP7 (LipidomicNet) [202272]
- Paulo Foundation
- Orion-Farmos Research Foundation
- University of Helsinki
- Finnish Atherosclerosis Society
- University of Helsinki Medicine Fund
- University of Helsinki Jubilee Fund
- Academy of Finland (AKA) [121457, 121457] Funding Source: Academy of Finland (AKA)
- Novo Nordisk Fonden [NNF11OC1014724] Funding Source: researchfish
Oxysterol-binding protein (OSBP) homologues, ORPs, are implicated in lipid homeostatic control, vesicle transport, and cell signaling. We analyzed here the quantity of ORP mRNAs in human subcutaneous (s.c.) and visceral adipose depots, as well as in the Simpson-Golabi-Behmel syndrome (SGBS) adipocyte cell model. All of the ORP mRNAs were present in the s.c and visceral adipose tissues, and the two depots shared an almost identical ORP mRNA expression pattern. SGBS adipocytes displayed a similar pattern, suggesting that the adipose tissue ORP expression pattern mainly derives from adipocytes. During SGBS cell adipogenic differentiation, ORP2, ORP3, ORP4, ORP7, and ORP8 mRNAs were down-regulated, while ORP11 was induced. To assess the impacts of ORPs on adipocyte differentiation, ORP3 and ORP8, proteins down-regulated during adipogenesis, were overexpressed in differentiating SGBS adipocytes, while ORP11, a protein induced during adipogenesis, was silenced. ORP8 overexpression resulted in reduced expression of the aP2 mRNA, while down-regulation of adiponectin and aP2 was observed in ORP11 silenced cells. Furthermore, ORP8 overexpression or silencing of ORP11 markedly decreased cellular triglyceride storage. These data identify the patterns of ORP expression in human adipose depots and SGBS adipocytes, and provide the first evidence for a functional impact of ORPs on the adipocyte phenotype.
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