IL-4 and IL-13 induce myofibroblastic phenotype of human lung fibroblasts through c-Jun NH2-terminal kinase-dependent pathway

Hashimoto, Shu; Gon, Yasuhiro; Takeshita, Ikuko; Maruoka, Shuichiro; Horie, Takashi

doi:10.1067/mai.2001.114702

Cited by 151Asthma and respiratory diseasesInterstitial Lung Diseases and Idiopathic Pulmonary FibrosisCardiac Fibrosis and Remodeling

IL-4 and IL-13 induce myofibroblastic phenotype of human lung fibroblasts through c-Jun NH2-terminal kinase-dependent pathway

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Hashimoto, Shu, Gon, Yasuhiro, Takeshita, Ikuko, Maruoka, Shuichiro, Horie, Takashi·2001·Journal of Allergy and Clinical Immunology

DOI 10.1067/mai.2001.114702

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Abstract

Background Myofibroblasts play a role in the airway remodeling response of bronchial asthma. IL-4 and IL-13 are possibly involved in the airway remodeling response by inducing extracellular matrix production by fibroblasts. However, the roles of these cytokines in inducing the phenotypic modulation of human lung fibroblasts (HLFs) to myofibroblasts and the intracellular signal have not been determined.Objective We examined the effect of IL-4 and IL-13 on inducing the phenotypic modulation of HLFs to myofibroblasts characterized by alpha-smooth muscle actin and examined the role of the mitogen-activated protein (MAP) kinase superfamily in inducing the myofibroblastic phenotype of the HLF to clarify these issues.Methods Phosphorylation and activities of c-Jun NH(2)-terminal kinase (JNK), p38 MAP kinase, and extracellular signal-regulated kinase (Erk) were examined by using Western blotting and in vitro kinase assay. Expression of alpha-smooth muscle actin in IL-4- and IL-13-stimulated HLFs was analyzed by means of Western blotting.Results The results showed that (1) IL-4 and IL-13 increased alpha-smooth muscle actin expression in a dose- and time-dependent manner; (2) IL-4 and IL-13 induced increases in JNK and Erk phosphorylation and activity but not p38 MAP kinase activity; (3) CEP-1347 and PD 98059 attenuated IL-4- and IL13-induced JNK and Erk activity, respectively; and (4) CEP-1347, but not PD 98059, attenuated IL-4- and IL-13-induced alpha-smooth muscle actin expression.Conclusion These results indicate that IL-4 and IL-13 are capable of inducing the phenotypic modulation of HLFs to myofibroblasts, and JNK, but not p38 MAP kinase and Erk, regulates IL-4- and IL-13-induced phenotypic modulation of HLFs to myofibroblasts.

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IL-4 and IL-13 are pro-fibrotic.
“In addition to these factors, both IL-4 and IL-13 are pro-fibrotic (150).”
From Unraveling SSc Pathophysiology; The Myofibroblast (2018) · cites this paper as [150]
Both IL-4 and IL-13 induce αSMA expression in primary lung fibroblasts in a dose- and time-dependent manner.
“Both cytokines induce αSMA expression in primary lung fibroblasts in a dose- and time-dependent manner (105, 150), and enhance the production of collagen type I in normal fibroblasts (108).”
From Unraveling SSc Pathophysiology; The Myofibroblast (2018) · cites this paper as [150]

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Authors: Hashimoto, S., Gon, Y., Takeshita, I., Maruoka, S., & Horie, T.
Affiliations: Nihon University (JP)
ORCID: Hashimoto, Shu
Maruoka, Shuichiro
Venue: Journal of Allergy and Clinical Immunology
Publisher: Elsevier BV
Published: 2001-06
Volume: 107
Issue: 6
Pages: 1001-1008
ISSN: 0091-6749 (ISSN-L)
DOI: 10.1067/mai.2001.114702
OpenAlex: W2129536790
Cited by: 151
References: 51
Citations by year: 2026: 2 · 2025: 12 · 2024: 8 · 2023: 10 · 2022: 5 · 2021: 8 · 2020: 10 · 2019: 6 · 2018: 9 · 2017: 4 · 2016: 10 · 2015: 2 · 2014: 2 · 2013: 1 · 2012: 2
FWCI: 5.30
Type: journal article
Language: en
Open access: bronze
doi.org
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations: Journal of Allergy and Clinical Immunology (publishedVersion)
PubMed (publishedVersion)
Topics: Health Sciences › Medicine › Physiology › Asthma and respiratory diseases
Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Interstitial Lung Diseases and Idiopathic Pulmonary Fibrosis
Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Fibrosis and Remodeling
Keywords: IL-4, IL-13, myofibroblasts, lung fibroblasts, c-Jun NH2-terminal kinase, MAPK signaling, alpha-smooth muscle actin, airway remodeling, asthma, extracellular matrix synthesis, CEP-1347, PD98059, p38 MAPK, ERK
MeSH terms: Actins, Carbazoles, Cell Differentiation, Cells, Cultured, Enzyme Inhibitors, Fibroblasts, Humans, Indoles, Lung, Muscle, Smooth, Phenotype, Interleukin-4, Interleukin-13, Mitogen-Activated Protein Kinases, JNK Mitogen-Activated Protein Kinases, p38 Mitogen-Activated Protein Kinases

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IL-4 and IL-13 induce myofibroblastic phenotype of human lung fibroblasts through c-Jun NH2-terminal kinase-dependent pathway

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