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Perivascular mesenchymal cells control adipose-tissue macrophage accrual in obesity. | LitMetric

AI Article Synopsis

  • Chronic low-grade inflammation in white adipose tissue (WAT) is a key feature of metabolic syndrome linked to obesity, driven by specific cell types.
  • Fibro-inflammatory progenitors (FIPs) in mouse WAT become activated by high-fat diets, promoting proinflammatory signals and macrophage accumulation via TLR4 pathways.
  • The transcription factor ZFP423 plays a crucial role in regulating this inflammation by inhibiting NF-κB signaling, and manipulating its expression can either suppress or exacerbate inflammatory responses in WAT.

Article Abstract

Chronic low-grade white adipose tissue (WAT) inflammation is a hallmark of metabolic syndrome in obesity. Here, we demonstrate that a subpopulation of mouse WAT perivascular (PDGFRβ) cells, termed fibro-inflammatory progenitors (FIPs), activate proinflammatory signalling cascades shortly after the onset of high-fat diet feeding and regulate proinflammatory macrophage accumulation in WAT in a TLR4-dependent manner. FIPs activation in obesity is mediated by the downregulation of zinc-finger protein 423 (ZFP423), identified here as a transcriptional corepressor of NF-κB. ZFP423 suppresses the DNA-binding capacity of the p65 subunit of NF-κB by inducing a p300-to-NuRD coregulator switch. Doxycycline-inducible expression of Zfp423 in PDGFRβ cells suppresses inflammatory signalling in FIPs and attenuates metabolic inflammation of visceral WAT in obesity. Inducible inactivation of Zfp423 in PDGFRβ cells increases FIP activity, exacerbates adipose macrophage accrual and promotes WAT dysfunction. These studies implicate perivascular mesenchymal cells as important regulators of chronic adipose-tissue inflammation in obesity and identify ZFP423 as a transcriptional break on NF-κB signalling.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7669663PMC
http://dx.doi.org/10.1038/s42255-020-00301-7DOI Listing

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