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Abstract

Intermittent hypoxia up regulates mTOR expression in hepatic macrophages through CX3CL1/CX3CR1

Background and Aim

mTOR pathway of hepatic macrophages (Kupffer cells) plays an important role in the development of MAFLD. The interaction between chemokine CX3CL1 secreted by hepatic stellate cells (HSC) and receptor CX3CR1 of hepatic macrophages may be the key link for these two cells to participate in liver injury. The aim of this study was to investigate whether intermittent hypoxia (IH), the main pathogenesis of OSA, is involved in liver injury through CX3CL1/CX3CR1 regulation of mTOR expression in macrophages.

Methods

Primary mouse hepatic stellate cells and primary macrophages were extracted and co cultured for 72 hours under IH in vitro (15% and 8% oxygen concentration for 5 minutes, then 21% oxygen concentration for 5 minutes, cycling). The protein expression of CX3CL1?CX3CR1 and mTOR were detected with WB.

Results

It was found that IH simultaneously increased the expression of CX3CL1 protein in HSCs, and the expression of CX3CR1 and mTOR in macrophages, which related with severity of IH. After blocking CX3CR1 on macrophages with antagonists, the increase of mTOR in macrophages was weakened by IH (Fig. 1). It is suggested that IH stimulates HSCs to up regulate macrophage mTOR through CX3CL1/CX3CR1 Conclusion

IH regulates mTOR expression in hepatic macrophages through CX3CL1/CX3CR1, which may be an important mechanism of MAFLD induced by OSA.

Fig. 1 (1) control group (normal air),(2) 15% IH+CX3CR1 antagonists group,(3) 8% IH+CX3CR1 antagonists group,(4) 15% IH group,(5) 8% IH group

Abstract

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