TM4SF5-dependent crosstalk between hepatocytes and macrophages to reprogram the inflammatory environment

Summary: Chronic injury to hepatocytes results in inflammation, steatohepatitis, fibrosis, and nonalcoholic fatty liver disease (NAFLD). The tetraspanin TM4SF5 is implicated in fibrosis and cancer. We investigate the role of TM4SF5 in communication between hepatocytes and macrophages (MΦs) and its p...

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Autores principales:	Eunmi Kim, Hyejin Um, Jinsoo Park, Jae Woo Jung, Ji Eon Kim, Haesong Lee, Eun-Ae Shin, Yangie Pinanga, Hyejin Lee, Seo Hee Nam, Jung Weon Lee
Formato:	article
Lenguaje:	EN
Publicado:	Elsevier 2021
Materias:	cytokines/chemokines diet animal model fibrosis glycolysis hepatocytes inflammation Biology (General) QH301-705.5
Acceso en línea:	https://doaj.org/article/30bc3a81cc954bfe861f776a7c275d30
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spelling	oai:doaj.org-article:30bc3a81cc954bfe861f776a7c275d302021-11-18T04:47:58ZTM4SF5-dependent crosstalk between hepatocytes and macrophages to reprogram the inflammatory environment2211-124710.1016/j.celrep.2021.110018https://doaj.org/article/30bc3a81cc954bfe861f776a7c275d302021-11-01T00:00:00Zhttp://www.sciencedirect.com/science/article/pii/S221112472101500Xhttps://doaj.org/toc/2211-1247Summary: Chronic injury to hepatocytes results in inflammation, steatohepatitis, fibrosis, and nonalcoholic fatty liver disease (NAFLD). The tetraspanin TM4SF5 is implicated in fibrosis and cancer. We investigate the role of TM4SF5 in communication between hepatocytes and macrophages (MΦs) and its possible influence on the inflammatory microenvironment that may lead to NAFLD. TM4SF5 induction in differentiated MΦs promotes glucose uptake, glycolysis, and glucose sensitivity, leading to M1-type MΦ activation. Activated M1-type MΦs secrete pro-inflammatory interleukin-6 (IL-6), which induces the secretion of CCL20 and CXCL10 from TM4SF5-positive hepatocytes. Although TM4SF5-dependent secretion of these chemokines enhances glycolysis in M0 MΦs, further chronic exposure reprograms MΦs for an increase in the proportion of M2-type MΦs in the population, which may support diet- and chemical-induced NAFLD progression. We suggest that TM4SF5 expression in MΦs and hepatocytes is critically involved in modulating the inflammatory environment during NAFLD progression.Eunmi KimHyejin UmJinsoo ParkJae Woo JungJi Eon KimHaesong LeeEun-Ae ShinYangie PinangaHyejin LeeSeo Hee NamJung Weon LeeElsevierarticlecytokines/chemokinesdiet animal modelfibrosisglycolysishepatocytesinflammationBiology (General)QH301-705.5ENCell Reports, Vol 37, Iss 7, Pp 110018- (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	cytokines/chemokines diet animal model fibrosis glycolysis hepatocytes inflammation Biology (General) QH301-705.5
spellingShingle	cytokines/chemokines diet animal model fibrosis glycolysis hepatocytes inflammation Biology (General) QH301-705.5 Eunmi Kim Hyejin Um Jinsoo Park Jae Woo Jung Ji Eon Kim Haesong Lee Eun-Ae Shin Yangie Pinanga Hyejin Lee Seo Hee Nam Jung Weon Lee TM4SF5-dependent crosstalk between hepatocytes and macrophages to reprogram the inflammatory environment
description	Summary: Chronic injury to hepatocytes results in inflammation, steatohepatitis, fibrosis, and nonalcoholic fatty liver disease (NAFLD). The tetraspanin TM4SF5 is implicated in fibrosis and cancer. We investigate the role of TM4SF5 in communication between hepatocytes and macrophages (MΦs) and its possible influence on the inflammatory microenvironment that may lead to NAFLD. TM4SF5 induction in differentiated MΦs promotes glucose uptake, glycolysis, and glucose sensitivity, leading to M1-type MΦ activation. Activated M1-type MΦs secrete pro-inflammatory interleukin-6 (IL-6), which induces the secretion of CCL20 and CXCL10 from TM4SF5-positive hepatocytes. Although TM4SF5-dependent secretion of these chemokines enhances glycolysis in M0 MΦs, further chronic exposure reprograms MΦs for an increase in the proportion of M2-type MΦs in the population, which may support diet- and chemical-induced NAFLD progression. We suggest that TM4SF5 expression in MΦs and hepatocytes is critically involved in modulating the inflammatory environment during NAFLD progression.
format	article
author	Eunmi Kim Hyejin Um Jinsoo Park Jae Woo Jung Ji Eon Kim Haesong Lee Eun-Ae Shin Yangie Pinanga Hyejin Lee Seo Hee Nam Jung Weon Lee
author_facet	Eunmi Kim Hyejin Um Jinsoo Park Jae Woo Jung Ji Eon Kim Haesong Lee Eun-Ae Shin Yangie Pinanga Hyejin Lee Seo Hee Nam Jung Weon Lee
author_sort	Eunmi Kim
title	TM4SF5-dependent crosstalk between hepatocytes and macrophages to reprogram the inflammatory environment
title_short	TM4SF5-dependent crosstalk between hepatocytes and macrophages to reprogram the inflammatory environment
title_full	TM4SF5-dependent crosstalk between hepatocytes and macrophages to reprogram the inflammatory environment
title_fullStr	TM4SF5-dependent crosstalk between hepatocytes and macrophages to reprogram the inflammatory environment
title_full_unstemmed	TM4SF5-dependent crosstalk between hepatocytes and macrophages to reprogram the inflammatory environment
title_sort	tm4sf5-dependent crosstalk between hepatocytes and macrophages to reprogram the inflammatory environment
publisher	Elsevier
publishDate	2021
url	https://doaj.org/article/30bc3a81cc954bfe861f776a7c275d30
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TM4SF5-dependent crosstalk between hepatocytes and macrophages to reprogram the inflammatory environment

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