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An inducible sphingosine kinase 1 in hepatic stellate cells potentiates liver fibrosis. | LitMetric

An inducible sphingosine kinase 1 in hepatic stellate cells potentiates liver fibrosis.

Biochem Pharmacol

Department of Biomedical Science, College of Natural Science, Chosun University, Gwangju 61452, Republic of Korea; Department of Integrative Biological Sciences & BK21 FOUR Educational Research Group for Age-associated Disorder Control Technology, Chosun University, Gwangju 61452, Republic of Korea; Institute of Well-Aging Medicare & Chosun University G-LAMP Project Group, Chosun University, Gwangju 61452, Republic of Korea. Electronic address:

Published: November 2024

AI Article Synopsis

Article Abstract

Hepatic stellate cells (HSCs) play a role in hepatic fibrosis and sphingosine kinase (SphK) is involved in biological processes. As studies on the regulatory mechanisms and functions of SphK in HSCs during liver fibrosis are currently limited, this study aimed to elucidate the regulatory mechanism and connected pathways of SphK upon HSC activation. The expression of SphK1 was higher in HSCs than in hepatocytes, and upregulated in activated primary HSCs. SphK1 was also increased in liver homogenates of carbon tetrachloride-treated or bile duct ligated mice and in transforming growth factor-β (TGF-β)-treated LX-2 cells. TGF-β-mediated SphK1 induction was due to Smad3 signaling in LX-2 cells. SphK1 modulation altered the expression of liver fibrogenesis-related genes. This SphK1-mediated profibrogenic effect was dependent on SphK1/sphingosine-1-phosphate/sphingosine-1-phosphate receptor signaling through ERK. Epigallocatechin gallate blocked TGF-β-induced SphK1 expression and hepatic fibrogenesis by attenuating Smad and MAPK activation. SphK1 induced by TGF-β facilitates HSC activation and liver fibrogenesis, which is reversed by epigallocatechin gallate. Accordingly, SphK1 and related signal transduction may be utilized to treat liver fibrosis.

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Source
http://dx.doi.org/10.1016/j.bcp.2024.116520DOI Listing

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