scholarly journals Additive Effects of MicroRNAs and Transcription Factors on CCL2 Production in Human White Adipose Tissue

Diabetes ◽  
2013 ◽  
Vol 63 (4) ◽  
pp. 1248-1258 ◽  
Author(s):  
A. Kulyte ◽  
Y. Belarbi ◽  
S. Lorente-Cebrian ◽  
C. Bambace ◽  
E. Arner ◽  
...  
2021 ◽  
Vol 131 (19) ◽  
Author(s):  
Erica P. Homan ◽  
Bruna B. Brandão ◽  
Samir Softic ◽  
Abdelfattah El Ouaamari ◽  
Brian T. O’Neill ◽  
...  

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Jessica E. C. Jones ◽  
Nabil Rabhi ◽  
Joseph Orofino ◽  
Ramya Gamini ◽  
Valentina Perissi ◽  
...  

AbstractVisceral white adipose tissue (vWAT) expands and undergoes extensive remodeling during diet-induced obesity. Much is known about the contribution of various stromal vascular cells to the remodeling process, but less is known of the changes that occur within the adipocyte as it becomes progressively dysfunctional. Here, we performed a transcriptome analysis of isolated vWAT adipocytes to assess global pathway changes occurring in response to a chronic high fat diet (HFD). The data demonstrate that the adipocyte responds to the HFD by adopting a fibroblast-like phenotype, characterized by enhanced expression of ECM, focal adhesion and cytoskeletal genes and suppression of many adipocyte programs most notably those associated with mitochondria. This study reveals that during obesity the adipocyte progressively becomes metabolically dysfunctional due to its acquisition of fibrogenic functions. We propose that mechano-responsive transcription factors such as MRTFA and SRF contribute to both upregulation of morphological genes as well as suppression of mitochondrial programs.


2008 ◽  
Vol 295 (1) ◽  
pp. C213-C220 ◽  
Author(s):  
Fei Wang ◽  
Qiang Tong

PU.1 transcription factor is a critical regulator of hematopoiesis and leukemogenesis. Because PU.1 interacts with transcription factors GATA-2 and C/EBPα, and both are involved in the regulation of adipogenesis, we investigated whether PU.1 plays a role in the regulation of adipocyte differentiation. Our data indicate that PU.1 is expressed in white adipose tissue. PU.1 protein can also be detected in cultured 3T3-L1 adipocytes. Forced expression of PU.1 in 3T3-L1 cells inhibits adipocyte differentiation, whereas deletion of the transactivation domain of PU.1 abolishes this effect. The inhibition of adipocyte differentiation by PU.1 is achieved, at least in part, through repression of the transcriptional activity of C/EBPα and C/EBPβ. Furthermore, GATA-2 and PU.1 have an additive inhibitory effect on C/EBP transactivation and adipogenesis. Finally, the expression of PU.1 is increased in white adipose of obese mice.


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