Hepatic CD147 knockout modulates liver steatosis and up-regulates autophagy in high-fat-diet-induced NAFLD mice

Lou, Jiaxin; Li, Can; Li, Zengshan; Zhang, Tian; Chen, Zhi‐Nan; Bian, Huijie

doi:10.1016/j.bbrc.2020.01.164

Cited by 9 publications

(2 citation statements)

References 24 publications

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“…CD147 has been shown to regulate autophagy. In nonalcoholic fatty liver disease (NAFLD) mice, CD147-knockout can induce changes in liver autophagy (Lou et al 2020 ). The small molecule AC-73 is a specific inhibitor of CD147, which can inhibit the proliferation of leukemia cells and induce autophagy by blocking ERK/STAT3 signaling pathway (Spinello et al 2019 ).…”

Section: Discussionmentioning

confidence: 99%

Lipopolysaccharide induces inflammatory microglial activation through CD147-mediated matrix metalloproteinase expression

Yao

Liu

Tang

et al. 2022

Environ Sci Pollut Res

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Microglia-mediated neuroinflammation plays a vital role in the pathophysiological processes of multiple neurodegenerative diseases. Lipopolysaccharide (LPS) is an environmental poison that can induce inflammatory microglial activation. Matrix metalloproteinases (MMPs) are vital factors regulating microglial activation, and CD147 is a key MMP inducer, which can induce inflammation by inducing MMPs. However, whether it is involved in the regulation of microglial activation has not been reported. In this study, the role of CD147 in LPS-induced microglial inflammatory activation was investigated by establishing in vivo and in vitro models. The results suggested that LPS-induced microglial activation was accompanied by the induction of CD147 expression while the inhibition of CD147 expression could inhibit LPS-induced microglial inflammatory activation. In addition, the results also indicated that the role of CD147 in LPS-induced pro-inflammatory activation of microglia was related to its downstream MMP-3, MMP-8, and autophagy. Furthermore, the inhibition of MMP-3, MMP-8, and autophagy attenuated LPS-induced inflammatory activation of microglia. At the same time, there was a certain interaction between MMPs and autophagy, which is shown that inhibiting the expression of MMPs could inhibit autophagy, whereas inhibiting autophagy could inhibit the expression of MMPs. Taken together, we provided the first evidence that CD147/MMPs can be involved in LPS-induced inflammatory activation of microglia through an autophagy-dependent manner. Supplementary Information The online version contains supplementary material available at 10.1007/s11356-022-24292-y.

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Section: Discussionmentioning

confidence: 99%

Lipopolysaccharide induces inflammatory microglial activation through CD147-mediated matrix metalloproteinase expression

Yao

Liu

Tang

et al. 2022

Environ Sci Pollut Res

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“…In the present study, we found that BSG inhibition had the potential to ameliorate insulin resistance and hepatic steatosis. Other investigators demonstrated that CD147/BSG is associated with hepatic steatosis and autophagy in both patients with NAFLD and liver-specific Bsg -/mice (36). The differences between parts of the results of these 2 studies may be due to the Figure 6.…”

Section: Discussionmentioning

confidence: 94%

Basigin deficiency prevents anaplerosis and ameliorates insulin resistance and hepatosteatosis

Ryuge

Kosugi²,

Maeda³

et al. 2021

JCI Insight

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Hepatic autophagy fluctuates during the development of non-alcoholic fatty liver disease

Ding

Tseng

et al. 2020

Annals of Hepatology

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Hepatic CD147 knockout modulates liver steatosis and up-regulates autophagy in high-fat-diet-induced NAFLD mice

Cited by 9 publications

References 24 publications

Lipopolysaccharide induces inflammatory microglial activation through CD147-mediated matrix metalloproteinase expression

Lipopolysaccharide induces inflammatory microglial activation through CD147-mediated matrix metalloproteinase expression

Basigin deficiency prevents anaplerosis and ameliorates insulin resistance and hepatosteatosis

Hepatic autophagy fluctuates during the development of non-alcoholic fatty liver disease

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