Dataset Information

Expression of GPR43 in Brown Adipogenesis Is Enhanced by Rosiglitazone and Controlled by PPAR?/RXR Heterodimerization.

ABSTRACT: GPR43, a G-protein coupled receptor recognizing short-chain fatty acids, has been reported to participate in many biological functions of white adipocytes, such as adipogenesis and lipolysis. However, the functional role of GPR43 in brown adipocytes is still not clear. In this study, we investigated the effects of the PPAR? agonist rosiglitazone on GPR43 expression in brown adipogenesis. The results demonstrated that GPR43 was expressed during the late phase of brown adipocyte differentiation, which could be further augmented by adipogenic agent rosiglitazone treatment. The PPAR?/RXR heterodimerization was found to be the key transcription factor for this enhancing effect of rosiglitazone on GPR43 expression. Taken together, these results suggested GPR43 levels might be regulated by PPAR?-activated events during brown adipocytes differentiation and reflect the adipogenesis status of brown adipocytes.

SUBMITTER: Hu J

PROVIDER: S-EPMC5976906 | biostudies-literature | 2018

REPOSITORIES: biostudies-literature

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Expression of GPR43 in Brown Adipogenesis Is Enhanced by Rosiglitazone and Controlled by PPAR<i>γ</i>/RXR Heterodimerization.

Hu Jiamiao J Zhou Arong A Cheung Peter C K PCK Zheng Baodong B Zeng Shaoxiao S Lin Shaoling S

PPAR research 20180516

GPR43, a G-protein coupled receptor recognizing short-chain fatty acids, has been reported to participate in many biological functions of white adipocytes, such as adipogenesis and lipolysis. However, the functional role of GPR43 in brown adipocytes is still not clear. In this study, we investigated the effects of the PPAR<i>γ</i> agonist rosiglitazone on GPR43 expression in brown adipogenesis. The results demonstrated that GPR43 was expressed during the late phase of brown adipocyte differentia ...[more]

PMID: 29861709

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Project description:BACKGROUND: Nuclear receptors (NR) regulate transcription of genes involved in many biological processes such as development, cell proliferation, differentiation and cell death. Amongst them, PPARG2 and THR control tissue glucose and lipid homeostasis which are deregulated in severe pathophysiological conditions such as metabolic syndromes. METHODOLOGY/PRINCIPAL FINDINGS: Here, we describe a real time BRET approach to monitor heterodimerization between RXR and PPARG2 or THR in vitro or in living cells. The presence of a specific DNA target was required to induce in vitro a BRET shift reflecting heterodimerization of RXR/PPARG2 or RXR/THR. As in electrophoretic mobility shift assay (EMSA), the stringency and specificity of the BRET shift assay depended upon assay condition optimization including MgCl2 concentration. For the nuclear receptors, we found by mutagenesis analysis that each heterodimer partner must harbor an intact DNA binding domain to induce BRET and heterodimerization on a DNA target. Moreover the interaction between the PPARG2 ligand binding domain and the RXR DNA binding domain stabilized the heterodimer on its DNA target. BRET microscopy in living cells highlighted the heterodimerization of RXR/PPARG2 within the nucleus clustered in discrete foci that may represent active target gene transcription regulation regions. BRET imaging also suggested that heterodimerization between RXR and PPARG2 required the DNA binding of PPARG2. CONCLUSIONS/SIGNIFICANCE: The BRET approach described here allowed us to study the dynamic interactions which exist between NR in vitro or in living cells and can provide important information on heterodimerization modes, affinity with a given RE and subcellular localization of the heterodimers. This method could be used to study real time changes of NR heterodimers occurring on DNA depending upon cell activation, chromatin state and help to define the mechanisms of ligands or drug action designed to target NRs.

Dataset Information

Expression of GPR43 in Brown Adipogenesis Is Enhanced by Rosiglitazone and Controlled by PPAR?/RXR Heterodimerization.

Publications

Expression of GPR43 in Brown Adipogenesis Is Enhanced by Rosiglitazone and Controlled by PPAR<i>γ</i>/RXR Heterodimerization.

Similar Datasets

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