BMPR2 promotes fatty acid oxidation and protects white adipocytes from cell death in mice.

Abstract

Adipocyte cell death is pathologically involved in both obesity and lipodystrophy. Inflammation and pro-inflammatory cytokines are generally regarded as inducers for adipocyte apoptosis, but whether some innate defects affect their susceptibility to cell death has not been extensively studied. Here, we found bone morphogenetic protein receptor type 2 (BMPR2) knockout adipocytes were prone to cell death, which involved both apoptosis and pyroptosis. BMPR2 deficiency in adipocytes inhibited phosphorylation of perilipin, a lipid-droplet-coating protein, and impaired lipolysis when stimulated by tumor necrosis factor (TNFα), which lead to failure of fatty acid oxidation and oxidative phosphorylation. In addition, impaired lipolysis was associated with mitochondria-mediated apoptosis and pyroptosis as well as elevated inflammation. These results suggest that BMPR2 is important for maintaining the functional integrity of adipocytes and their ability to survive when interacting with inflammatory factors, which may explain why adipocytes among individuals show discrepancy for death responses in inflammatory settings.

• Authors: Shuwen Qian, Jiabao Pan, Yan Su, Yan Tang, Yina Wang, Ying Zou, Yaxin Zhao, Hong Ma, Youyou Zhang, Yang Liu, Liang Guo, Qi-Qun Tang
• Journal: Communications biology (Commun Biol) Vol. 3 Issue 1 Pg. 200 (04 29 2020) ISSN: 2399-3642 [Electronic] England
• PMID: 32350411 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Fatty Acids
• Bmpr2 protein, mouse
• Bone Morphogenetic Protein Receptors, Type II

Topics

• Adipocytes, White (metabolism)
• Adult
• Animals
• Bone Morphogenetic Protein Receptors, Type II (deficiency, metabolism)
• Cell Death
• Fatty Acids (metabolism)
• Female
• Humans
• Male
• Mice
• Mice, Knockout
• Middle Aged
• Oxidation-Reduction