Intercellular Communication between Hepatic Cells in Liver Diseases

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Abstract

Liver diseases are perpetuated by the orchestration of hepatocytes and other hepatic non-parenchymal cells. These cells communicate and regulate with each other by secreting mediators such as peptides, hormones, and cytokines. Extracellular vesicles (EVs), small particles secreted from cells, contain proteins, DNAs, and RNAs as cargos. EVs have attracted recent research interests since they can communicate information from donor cells to recipient cells thereby regulating physiological events via delivering of specific cargo mediators. Previous studies have demonstrated that liver cells secrete elevated numbers of EVs during diseased conditions, and those EVs are internalized into other liver cells inducing disease-related reactions such as inflammation, angiogenesis, and fibrogenesis. Reactions in recipient cells are caused by proteins and RNAs carried in disease-derived EVs. This review summarizes cell-to-cell communication especially via EVs in the pathogenesis of liver diseases and their potential as a novel therapeutic target.

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Most cited references 58

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Macrophage plasticity, polarization, and function in health and disease.

Fatemeh Mardani, Abbas Shapouri-Moghaddam, Saeed Mohammadian … (2018)

Macrophages are heterogeneous and their phenotype and functions are regulated by the surrounding micro-environment. Macrophages commonly exist in two distinct subsets: 1) Classically activated or M1 macrophages, which are pro-inflammatory and polarized by lipopolysaccharide (LPS) either alone or in association with Th1 cytokines such as IFN-γ, GM-CSF, and produce pro-inflammatory cytokines such as interleukin-1β (IL-1β), IL-6, IL-12, IL-23, and TNF-α; and 2) Alternatively activated or M2 macrophages, which are anti-inflammatory and immunoregulatory and polarized by Th2 cytokines such as IL-4 and IL-13 and produce anti-inflammatory cytokines such as IL-10 and TGF-β. M1 and M2 macrophages have different functions and transcriptional profiles. They have unique abilities by destroying pathogens or repair the inflammation-associated injury. It is known that M1/M2 macrophage balance polarization governs the fate of an organ in inflammation or injury. When the infection or inflammation is severe enough to affect an organ, macrophages first exhibit the M1 phenotype to release TNF-α, IL-1β, IL-12, and IL-23 against the stimulus. But, if M1 phase continues, it can cause tissue damage. Therefore, M2 macrophages secrete high amounts of IL-10 and TGF-β to suppress the inflammation, contribute to tissue repair, remodeling, vasculogenesis, and retain homeostasis. In this review, we first discuss the basic biology of macrophages including origin, differentiation and activation, tissue distribution, plasticity and polarization, migration, antigen presentation capacity, cytokine and chemokine production, metabolism, and involvement of microRNAs in macrophage polarization and function. Secondly, we discuss the protective and pathogenic role of the macrophage subsets in normal and pathological pregnancy, anti-microbial defense, anti-tumor immunity, metabolic disease and obesity, asthma and allergy, atherosclerosis, fibrosis, wound healing, and autoimmunity.

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Karim Si-Tayeb, Frédéric Lemaigre, Stephen Duncan (2010)

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Regulation of PDGF and its receptors in fibrotic diseases.

James C. Bonner (2004)

Platelet-derived growth factor (PDGF) isoforms play a major role in stimulating the replication, survival, and migration of myofibroblasts during the pathogenesis of fibrotic diseases. During fibrogenesis, PDGF is secreted by a variety of cell types as a response to injury, and many pro-inflammatory cytokines mediate their mitogenic effects via the autocrine release of PDGF. PDGF action is determined by the relative expression of PDGF alpha-receptors (PDGFRalpha) and beta-receptors (PDGFRbeta) on the surface of myofibroblasts. These receptors are induced during fibrogenesis, thereby amplifying biological responses to PDGF isoforms. PDGF action is also modulated by extracellular binding proteins and matrix molecules. This review summarizes the literature on the role of PDGF and its receptors in the development of fibrosis in a variety of organ systems, including lung, liver, kidney, and skin.

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Author and article information

Journal

Journal ID (nlm-ta): Int J Mol Sci

Journal ID (iso-abbrev): Int J Mol Sci

Journal ID (publisher-id): ijms

Title: International Journal of Molecular Sciences

Publisher: MDPI

ISSN (Electronic): 1422-0067

Publication date (Electronic): 02 May 2019

Publication date Collection: May 2019

Volume: 20

Issue: 9

Electronic Location Identifier: 2180

Affiliations

[1 ]Richard L. Roudebush VA Medical Center, Indianapolis, IN 46202, USA; keisato@ 123456iu.edu (K.S.); linkenn@ 123456iu.edu (L.K.); sliangpu@ 123456iu.edu (S.L.); pkusuman@ 123456iu.edu (P.K.); yangjoe@ 123456iu.edu (Z.Y.); mengf@ 123456iu.edu (F.M.); heafranc@ 123456iu.edu (H.F.)

[2 ]Indiana Center for Liver Research, Division of Gastroenterology & Hepatology, Department of Medicine, Indiana University School of Medicine, Indianapolis, IN 46202, USA

[3 ]Department of Medical Physiology, Texas A&M University, Temple, TX 76504, USA; SGlaser@ 123456medicine.tamhsc.edu

Author notes

[* ]Correspondence: galpini@ 123456iu.edu

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Keisaku Sato https://orcid.org/0000-0001-5380-8001

Article

Publisher ID: ijms-20-02180

DOI: 10.3390/ijms20092180

PMC ID: 6540342

PubMed ID: 31052525

SO-VID: c9b27397-ffa1-4823-8990-a5527bb1b653

License:

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

Intercellular Communication between Hepatic Cells in Liver Diseases

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Abstract

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Bacterial extracellular vesicles

Most cited references 58

Macrophage plasticity, polarization, and function in health and disease.

Organogenesis and development of the liver.

Regulation of PDGF and its receptors in fibrotic diseases.

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