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Expression patterns of transcription factor PPARγ and C/EBP family members during in vitro adipogenesis of human bone marrow mesenchymal stem cells
Author(s) -
Zhao XiaoYi,
Chen XiaoYong,
Zhang ZiJi,
Kang Yan,
Liao WeiMing,
Yu WeiHua,
Xiang Andy Peng
Publication year - 2015
Publication title -
cell biology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.932
H-Index - 77
eISSN - 1095-8355
pISSN - 1065-6995
DOI - 10.1002/cbin.10415
Subject(s) - adipogenesis , mesenchymal stem cell , peroxisome proliferator activated receptor , microbiology and biotechnology , endocrinology , biology , medicine , ccaat enhancer binding proteins , transcription factor , adipose tissue , adipocyte , bone marrow , mapk/erk pathway , ibmx , chemistry , signal transduction , receptor , immunology , biochemistry , forskolin , dna binding protein , gene , stimulation
In the past decades increasing lines of evidence have demonstrated that adipose tissue, as an endocrine organ plays a central role in metabolic homeostasis and its related maladies. CCAAT/enhancer‐binding protein (C/EBP) family members and the nuclear receptor peroxisome proliferator‐activated receptor gamma (PPARγ) were known to be the vital transcription factors in the regulation of adipogenesis. However, the exact mechanism for increased marrow fat in patients with bone metabolic diseases, such as osteoporosis, is still poorly understood. Herein, we studied the expression pattern of PPARγ and C/EBPs in human bone marrow mesenchymal stem cell (hBMSC) adipogenesis and evaluated the effects of individual components of an adipogenic cocktail on the differentiation and transcription factor expression. We furthermore examined whether the ERK signaling pathway was involved in mediating these effects. These findings showed that C/EBPβ and C/EBPδ were detected in undifferentiated hBMSC and maintained during the whole process of adipogenesis, and could initiate the expression of PPARγ1 under the treatment of dexamethasone and IBMX. Subsequently, the activation of PPARγ1 by indomethacin, its exogenous ligand, activated C/EBPα, which, together with IBMX, up‐regulated PPARγ2 expression and therefore the fullest adipogenesis. Insulin and its downstream signal pathway extracellular signal‐regulated kinases (ERK), however, were found not necessary for hBMSC adipogenesis. Our results revealed some unique characteristics of human adipocyte formation, which may help to understand the molecular mechanisms of bone marrow adipogenesis and give insights into the treatment of osteoporosis.