EGFR-mediated activation of adipose tissue macrophages promotes obesity and insulin resistance

Shirong Cao, Yu Pan, Jiaqi Tang, Andrew S. Terker, Juan Pablo Arroyo Ornelas, Guan-nan Jin, Yinqiu Wang, Aolei Niu, Xiaofeng Fan, Suwan Wang, Raymond C. Harris () and Ming-Zhi Zhang ()
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Shirong Cao: Vanderbilt University Medical Center
Yu Pan: Vanderbilt University Medical Center
Jiaqi Tang: Vanderbilt University Medical Center
Andrew S. Terker: Vanderbilt University Medical Center
Juan Pablo Arroyo Ornelas: Vanderbilt University Medical Center
Guan-nan Jin: Vanderbilt University Medical Center
Yinqiu Wang: Vanderbilt University Medical Center
Aolei Niu: Vanderbilt University Medical Center
Xiaofeng Fan: Vanderbilt University Medical Center
Suwan Wang: Vanderbilt University Medical Center
Raymond C. Harris: Vanderbilt University Medical Center
Ming-Zhi Zhang: Vanderbilt University Medical Center

Nature Communications, 2022, vol. 13, issue 1, 1-16

Abstract: Abstract Obesity and obesity-related health complications are increasing in prevalence. Adipose tissue from obese subjects has low-grade, chronic inflammation, leading to insulin resistance. Adipose tissue macrophages (ATMs) are a source of proinflammatory cytokines that further aggravate adipocyte dysfunction. In response to a high fat diet (HFD), ATM numbers initially increase by proliferation of resident macrophages, but subsequent increases also result from infiltration in response to chemotactic signals from inflamed adipose tissue. To elucidate the underlying mechanisms regulating the increases in ATMs and their proinflammatory phenotype, we investigated the role of activation of ATM epidermal growth factor receptor (EGFR). A high fat diet increased expression of EGFR and its ligand amphiregulin in ATMs. Selective deletion of EGFR in ATMs inhibited both resident ATM proliferation and monocyte infiltration into adipose tissue and decreased obesity and development of insulin resistance. Therefore, ATM EGFR activation plays an important role in adipose tissue dysfunction.

Date: 2022
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DOI: 10.1038/s41467-022-32348-3

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