Mitochondrial protein UCP1 mediates liver injury induced by LPS through EKR signaling pathway

P. Liu, J. Yang, Z.-Y. Chen, P. Zhang, G.-J. Shi

Department of Cadre Health Care, Qingdao Municipal Hospital, Qingdao, Shandong, China. guangjunshik@163.com

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• Gastroenterology

OBJECTIVE: Mitochondria are abundant in liver. The roles of mitochondrial protein in liver injury and related signaling pathways are still unclear. UCP1 is a novel mitochondrial transmembrane protein. Its expression pattern and function in liver still needs further investigation.

MATERIALS AND METHODS: A mouse model of liver injury was established by the treatment of LPS. UCP1 expression in the liver tissue was detected by Western blot and qRT-PCR. ERK signaling activity was tested by enzymatic activity kit. ATP production was evaluated by flow cytometry. Cell apoptosis was determined by Western blot and flow cytometry. ERK signaling pathway inhibitor, U0126, was used to pre-treat mice. Liver tissue from sepsis patients was collected from the surgery.

RESULTS: Our data showed that the level of UCP1 was upregulated, ERK signaling was activated, ATP production was reduced, and cell apoptosis was enhanced in mice with liver injury model caused by LPS. U0126 intervention significantly suppressed UCP1 expression, inhibited ERK signaling pathway, enhanced ATP production, and restrained liver cell apoptosis in mice liver injury model. UCP1 increased, ERK signaling activated, and cell apoptosis elevated in the liver tissue of sepsis patients.

CONCLUSIONS: UCP1 plays a role in the liver tissue of mouse liver injury model and sepsis patients through the modulation of mitochondrial ATP production and cell apoptosis by ERK signaling pathway.

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