scholarly journals Adipocyte Liver Kinase b1 Suppresses Beige Adipocyte Renaissance Through Class IIa Histone Deacetylase 4

Diabetes ◽  
2017 ◽  
Vol 66 (12) ◽  
pp. 2952-2963 ◽  
Author(s):  
Yangmeng Wang ◽  
Esther Paulo ◽  
Dongmei Wu ◽  
Yixuan Wu ◽  
Wendong Huang ◽  
...  
Keyword(s):  
Histone Deacetylase ◽  
Beige Adipocyte ◽  
Histone Deacetylase 4 ◽  
Liver Kinase B1

scholarly journals Adipocyte HDAC4 activation leads to beige adipocyte expansion and reduced adiposity

2018 ◽  
Vol 239 (2) ◽  
pp. 153-165 ◽  
Author(s):  
Esther Paulo ◽  
Dongmei Wu ◽  
Peter Hecker ◽  
Yun Zhang ◽  
Biao Wang
Keyword(s):  
Energy Homeostasis ◽  
Beige Adipocyte ◽  
Beige Adipocytes ◽  
Normal Chow ◽  
Histone Deacetylase 4 ◽  
Liver Kinase B1 ◽  
Metabolic Performance ◽  
Physiological Impact ◽  
Novel Strategy ◽  
Dependent Mechanism

Numerous studies have suggested that beige adipocyte abundance is correlated with improved metabolic performance, but direct evidence showing that beige adipocyte expansion protects animals from the development of obesity is missing. Previously, we have described that the liver kinase b1 (LKB1) regulates beige adipocyte renaissance in subcutaneous inguinal white adipose tissue (iWAT) through a class IIa histone deacetylase 4 (HDAC4)-dependent mechanism. This study investigates the physiological impact of persistent beige adipocyte renaissance in energy homeostasis in mice. Here we present that the transgenic mice H4-TG, overexpressing constitutively active HDAC4 in adipocytes, showed beige adipocyte expansion in iWAT at room temperature. H4-TG mice exhibited increased energy expenditure due to beige adipocyte expansion. They also exhibited reduced adiposity under both normal chow and high-fat diet (HFD) feeding conditions. Specific ablation of beige adipocytes reversed the protection against HFD-induced obesity in H4-TG mice. Taken together, our results directly demonstrate that beige adipocyte expansion regulates adiposity in mice and targeting beige adipocyte renaissance may present a novel strategy to tackle obesity in humans.

scholarly journals Histone deacetylase 4 mediates SMAD family member 4 deacetylation and induces 5-fluorouracil resistance in breast cancer cells

2013 ◽  
Vol 30 (3) ◽  
pp. 1293-1300 ◽  
Author(s):  
SEONG-LAN YU ◽  
DONG CHUL LEE ◽  
JI WOONG SON ◽  
CHANG GYO PARK ◽  
HOI YOUNG LEE ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Family Member ◽  
Histone Deacetylase ◽  
Breast Cancer Cells ◽  
Histone Deacetylase 4

scholarly journals Hydrogen Sulfide Protects Cardiomyocytes against Apoptosis in Ischemia/Reperfusion through MiR-1-Regulated Histone Deacetylase 4 Pathway

2016 ◽  
Vol 41 (1) ◽  
pp. 10-21 ◽  
Author(s):  
Bo Kang ◽  
Wei Li ◽  
Wang Xi ◽  
Yinghong Yi ◽  
Yundan Ciren ◽  
...  
Keyword(s):  
Hydrogen Sulfide ◽  
Protective Effect ◽  
Signaling Pathway ◽  
Tumor Cells ◽  
Histone Deacetylase ◽  
Caspase 3 ◽  
Ischemia Reperfusion ◽  
Underlying Mechanism ◽  
Neonatal Rats ◽  
Histone Deacetylase 4

Background/Aims: Hydrogen sulfide (H<Sub>2</Sub>S) is a powerful inhibitor of cardiomyocytes apoptosis following ischemia/reperfusion (IR) injury, but the underlying mechanism remains unclear. Our previous study showed that microRNA-1 (miR-1) was upregulated by 2.21 fold in the IR group compared with that in the H<Sub>2</Sub>S preconditioned group. MiR-206 affected the process of cardiomyocytes hypertrophy by regulating histone deacetylase 4 (HDAC4). HDAC4 is also known to play an anti-apoptotic role in tumor cells, but its role in the myocardium has not been reported. The aim of this study was to test whether H<Sub>2</Sub>S could inhibit apoptosis of cardiomyocytes through HDAC4 regulation by miR-1 in IR. Methods: Cardiomyocytes of neonatal rats were subjected to hypoxia/reoxygenation (HR) injury with or without H<Sub>2</Sub>S pretreatment to simulate IR injury Cardiomyocytes were transfected with miR-1 mimic or HDAC4 siRNA to evaluate whether the miR-1-HDAC4 signaling pathway was involved in the protective effect of H<Sub>2</Sub>S. Results: HR increased cell apoptosis and caspase-3 cleavage, upregulated miR-1, and downregulated HDAC4. H<Sub>2</Sub>S preconditioning attenuated the apoptosis of cardiomyocytes, caspase-3 cleavage and LDH release, and enhanced cell viability In addition, H<Sub>2</Sub>S downregulated miR-1, and preserved HDAC4 expression. HDAC4 protein was down-regulated by miR-1 mimic. Transfection of cardiomyocytes with miR-1 mimic partially reduced the protective effect of H<Sub>2</Sub>S. Meanwhile, transfection of cardiomyocytes with siRNA to HDAC4 partially abrogated the protective effect of H<Sub>2</Sub>S. Conclusions: The miR-1-HDAC4 signaling pathway is involved in the protective effect of H<Sub>2</Sub>S against the apoptosis of cardiomyocytes during the IR injury process.

scholarly journals Caspase-mediated Specific Cleavage of Human Histone Deacetylase 4

2004 ◽  
Vol 279 (33) ◽  
pp. 34537-34546 ◽  
Author(s):  
Fang Liu ◽  
Melissa Dowling ◽  
Xiang-Jiao Yang ◽  
Gary D. Kao
Keyword(s):  
Histone Deacetylase ◽  
Histone Deacetylase 4
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