Intercellular Transmission of Hepatic ER Stress in Obesity Disrupts Systemic Metabolism.
Intercellular Transmission of Hepatic ER Stress in Obesity Disrupts Systemic Metabolism.
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肥胖症中肝ER应力的细胞间传播破坏了系统性代谢。
DOI:
10.1016/j.cmet.2020.11.009
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发表时间:
2021-02-02
期刊:
影响因子:
29
通讯作者:
Hotamisligil GS
中科院分区:
文献类型:
--
作者:
Tirosh A;Tuncman G;Calay ES;Rathaus M;Ron I;Tirosh A;Yalcin A;Lee YG;Livne R;Ron S;Minsky N;Arruda AP;Hotamisligil GS
Endoplasmic reticulum stress (ERS) has a pathophysiological role in obesity-associated insulin resistance. Yet, the coordinated tissue response to ERS remains unclear. Increased connexin (Cx)43-mediated intercellular communication, has been implicated in tissue adaptive and maladaptive response to various chronic stresses. Here we demonstrate that in hepatocytes, ERS results in increased Cx43 expression and cell-cell coupling. Co-culture of ER stressed ‘donor’ cells resulted in inter-cellular transmission of ERS and dysfunction to ERS-naïve ‘recipient’ cells (‘bystander response’), which could be prevented by genetic or pharmacologic suppression of Cx43. Hepatocytes from obese mice were able to transmit ERS to hepatocytes from lean mice, and mice lacking liver Cx43 were protected from diet-induced ERS, insulin resistance, and hepatosteatosis. Taken together, our results indicate that in obesity, the increased Cx43-mediated cell-cell coupling allows inter-cellular propagation of ERS. This novel maladaptive response to over-nutrition exacerbates the tissue ERS burden, promoting hepatosteatosis and impairing whole-body glucose metabolism. Connexin-43 (Cx43) has a key role in cell-cell communication. While Cx43-mediated inter-cellular communication is an adaptive tissue response in acute stress, it may become deleterious under chronic, non-resolving stress conditions. Herein, Tirosh et al. discover that in obesity, Cx43 allows deleterious signals to disseminate between cells in the liver, leading to fatty-liver disease and metabolic alterations.
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影响因子:
8.8
作者:
Charles KN;Li MD;Engin F;Arruda AP;Inouye K;Hotamisligil GS
通讯作者:
Hotamisligil GS
DOI:
10.1093/bioinformatics/btu638
发表时间:
2015-01-15
期刊:
Bioinformatics (Oxford, England)
影响因子:
--
作者:
Anders S;Pyl PT;Huber W
通讯作者:
Huber W
影响因子:
--
作者:
Belousov AB;Fontes JD;Freitas-Andrade M;Naus CC
通讯作者:
Naus CC
影响因子:
3.3
作者:
Gunawardena J
通讯作者:
Gunawardena J
影响因子:
82.9
作者:
Iwawaki, T;Akai, R;Miura, M
通讯作者:
Miura, M