scholarly journals Role of the Nuclear Receptor Corepressor 1 (NCOR1) in Atherosclerosis and Associated Immunometabolic Diseases

2020 ◽  
Vol 11 ◽  
Author(s):  
Martin A. Geiger ◽  
Ana T. Guillaumon ◽  
Francesco Paneni ◽  
Christian M. Matter ◽  
Sokrates Stein
Hepatology ◽  
2018 ◽  
Vol 67 (3) ◽  
pp. 1071-1087 ◽  
Author(s):  
Qing Ou-Yang ◽  
Xi-Meng Lin ◽  
Yan-Jing Zhu ◽  
Bo Zheng ◽  
Liang Li ◽  
...  

Endocrinology ◽  
2010 ◽  
Vol 151 (3) ◽  
pp. 1212-1220 ◽  
Author(s):  
Heather M. Jessen ◽  
Mira H. Kolodkin ◽  
Meaghan E. Bychowski ◽  
Catherine J. Auger ◽  
Anthony P. Auger

Nuclear receptor function on DNA is regulated by the balanced recruitment of coregulatory complexes. Recruited proteins that increase gene expression are called coactivators, and those that decrease gene expression are called corepressors. Little is known about the role of corepressors, such as nuclear receptor corepressor (NCoR), on the organization of behavior. We used real-time PCR to show that NCoR mRNA levels are sexually dimorphic, that females express higher levels of NCoR mRNA within the developing amygdala and hypothalamus, and that NCoR mRNA levels are reduced by estradiol treatment. To investigate the functional role of NCoR on juvenile social behavior, we infused small interfering RNA targeted against NCoR within the developing rat amygdala and assessed the enduring impact on juvenile social play behavior, sociability, and anxiety-like behavior. As expected, control males exhibited higher levels of juvenile social play than control females. Reducing NCoR expression during development further increased juvenile play in males only. Interestingly, decreased NCoR expression within the developing amygdala had lasting effects on increasing juvenile anxiety-like behavior in males and females. These data suggest that the corepressor NCoR functions to blunt sex differences in juvenile play behavior, a sexually dimorphic and hormone-dependent behavior, and appears critical for appropriate anxiety-like behavior in juvenile males and females.


2012 ◽  
Vol 287 (45) ◽  
pp. 38295-38304 ◽  
Author(s):  
Zhaoting Wu ◽  
Meng Yang ◽  
Hongjie Liu ◽  
Hongchao Guo ◽  
Yuan Wang ◽  
...  

2010 ◽  
Vol 2010 ◽  
pp. 1-10 ◽  
Author(s):  
Lucía Fuentes ◽  
Tamás Rőszer ◽  
Mercedes Ricote

Visceral obesity is coupled to a general low-grade chronic inflammatory state characterized by macrophage activation and inflammatory cytokine production, leading to insulin resistance (IR). The balance between proinflammatory M1 and antiinflammatory M2 macrophage phenotypes within visceral adipose tissue appears to be crucially involved in the development of obesity-associated IR and consequent metabolic abnormalities. The ligand-dependent transcription factors peroxisome proliferator activated receptors (PPARs) have recently been implicated in the determination of the M1/M2 phenotype. Liver X receptors (LXRs), which form another subgroup of the nuclear receptor superfamily, are also important regulators of proinflammatory cytokine production in macrophages. Disregulation of macrophage-mediated inflammation by PPARs and LXRs therefore underlies the development of IR. This review summarizes the role of PPAR and LXR signaling in macrophages and current knowledge about the impact of these actions in the manifestation of IR and obesity comorbidities such as liver steatosis and diabetic osteopenia.


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