scholarly journals A Peroxisome Proliferator-response Element in the Murinemc2-rPromoter Regulates Its Transcriptional Activation during Differentiation of 3T3-L1 Adipocytes

2004 ◽  
Vol 279 (22) ◽  
pp. 22803-22808 ◽  
Author(s):  
Luke A. Noon ◽  
Adrian J. L. Clark ◽  
Peter J. King
2003 ◽  
Vol 311 (1) ◽  
pp. 149-155 ◽  
Author(s):  
Franck Hansmannel ◽  
Marie-Claude Clémencet ◽  
Catherine Le Jossic-Corcos ◽  
Takashi Osumi ◽  
Norbert Latruffe ◽  
...  

1995 ◽  
Vol 270 (33) ◽  
pp. 19269-19276 ◽  
Author(s):  
Kristina Schoonjans ◽  
Mitsuhiro Watanabe ◽  
Hiroyuki Suzuki ◽  
Abderrahim Mahfoudi ◽  
Grigorios Krey ◽  
...  

2005 ◽  
Vol 37 (2) ◽  
pp. 101-110 ◽  
Author(s):  
Seung-Soon Im ◽  
Jae-Woo Kim ◽  
Tae-Hyun Kim ◽  
Xian-Li Song ◽  
So-Youn Kim ◽  
...  

Endocrinology ◽  
2010 ◽  
Vol 151 (7) ◽  
pp. 3195-3203 ◽  
Author(s):  
Qinqiang Long ◽  
Ting Lei ◽  
Bin Feng ◽  
Changjun Yin ◽  
Dan Jin ◽  
...  

Adiponectin, an adipocyte-derived hormone, is a versatile player involved in the regulation of energy homeostasis, cardiovascular disease, and diabetes. Within adipocytes, adiponectin is retained in the lumen of the endoplasmic reticulum (ER) by binding to the thiol protein ER resident protein 44 kDa (ERp44), which is apparently regulated by the activation of nuclear receptor peroxisome proliferator-activated receptor (PPAR)-γ. However, the precise role of ERp44 in adiponectin secretion remains elusive. In the present study, we investigated the functional correlation between ERp44 and adiponectin in a pig model. The transcription of porcine ERp44 was regulated by PPARγ, which was consistent with the finding of putative peroxisome proliferator response element sites within ERp44 promoter. Using chromatin immunoprecipitation and luciferase reporter assays, we demonstrated that the transcription of porcine ERp44 is repressed through binding of PPARγ to a peroxisome proliferator response element site located between positions −981 and −1004 in its 5′-flanking region. In human embryonic kidney 293 cells stably transfected with cDNA encoding porcine adiponectin, the secretion of adiponectin was significantly up-regulated and the ERp44 mRNA was down-regulated observably, by either the treatment of PPARγ agonist rosiglitazone or the overexpression of PPARγ in these cells. Taken together, our results indicated that PPARγ is an essential regulatory factor for the transcriptional activity of ERp44, which in turn controls the secretion of adiponectin.


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