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β2-adrenergic receptor promotes liver regeneration partially through crosstalk with c-met
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Journal Article
β2-adrenergic receptor promotes liver regeneration partially through crosstalk with c-met
2022
Overview
The β
2
-adrenergic receptor (β
2
AR) is a G protein-coupled receptor (GPCR) that mediates the majority of cellular responses to external stimuli. Aberrant expression of β
2
AR results in various pathophysiological disorders, including tumorigenesis, but little is known about its role in liver regeneration. This study aims to investigate the impact and the underlying mechanism of β
2
AR in liver regeneration. Here, we found that β
2
AR was upregulated during liver regeneration induced by 70% PH. Deletion of β
2
AR in mice resulted in 62% mortality 2 days post-PH, decreased proliferative marker expression and impaired liver function throughout regeneration. Moreover, AAV8-mediated overexpression of β
2
AR in hepatocytes accelerated the regeneration process and increased target gene expression. Mechanistically, β
2
AR recruited G-protein-coupled receptor kinase 2 (GRK2) to the membrane and then formed a complex with c-met to transactivate c-met signaling, which triggered downstream extracellular regulated protein kinase (ERK) signaling activation and nuclear translocation. Inhibition of c-met with SU11274 or ERK with U0126 decreased β
2
AR overexpression-induced hepatocyte proliferation. Our findings revealed that β
2
AR might act as a critical mediator regulating liver regeneration by crosstalk with c-met and activation of ERK signaling.
Publisher
Nature Publishing Group UK,Springer Nature B.V,Nature Publishing Group
Subject
