Interleukin-10 gene therapy reverses thioacetamide-induced liver fibrosis in mice

Kung Sheng Hung, Tsung Hsing Lee, Wen Ying Chou, Chia Ling Wu, Chung Lung Cho, Cheng Nan Lu, Bruno Jawan, Cheng Haung Wang

Research output: Contribution to journalArticle

45 Citations (Scopus)

Abstract

Hepatic fibrosis represents a process of healing and scarring in response to chronic liver injury. Interleukin-10 (IL-10) is a cytokine that downregulates the proinflammatory response and has a modulatory effect on hepatic fibrogenesis. The aim of this study was to investigate whether IL-10 gene therapy possesses anti-hepatic fibrogenesis in mice. Liver fibrosis was induced by long-term thioacetamide administration in mice. Human IL-10 expression plasmid was delivered via electroporation after liver fibrosis established. IL-10 gene therapy reversed hepatic fibrosis and prevented cell apoptosis in a thioacetamide-treated liver. RT-PCR revealed IL-10 gene therapy to reduce liver transforming growth factor-β1, tumor necrosis factor-α, collagen α1, cell adhesion molecule, and tissue inhibitors of metalloproteinase mRNA upregulation. Following gene transfer, the activation of α-smooth muscle actin and cyclooxygenase-2 was significantly attenuated. In brief, IL-10 gene therapy might be an effective therapeutic reagent for liver fibrosis with potential future clinical applications.

Original languageEnglish
Pages (from-to)324-331
Number of pages8
JournalBiochemical and Biophysical Research Communications
Volume336
Issue number1
DOIs
Publication statusPublished - Oct 14 2005
Externally publishedYes

Fingerprint

Thioacetamide
Gene therapy
Liver Cirrhosis
Genetic Therapy
Liver
Interleukin-10
Fibrosis
Gene transfer
Tissue Inhibitor of Metalloproteinases
Electroporation
Cell Adhesion Molecules
Transforming Growth Factors
Cyclooxygenase 2
Cicatrix
Smooth Muscle
Muscle
Actins
Plasmids
Up-Regulation
Collagen

Keywords

  • COX-2
  • Gene therapy
  • IL-10
  • Liver fibrosis
  • Thioacetamide

ASJC Scopus subject areas

  • Biochemistry
  • Biophysics
  • Molecular Biology

Cite this

Interleukin-10 gene therapy reverses thioacetamide-induced liver fibrosis in mice. / Hung, Kung Sheng; Lee, Tsung Hsing; Chou, Wen Ying; Wu, Chia Ling; Cho, Chung Lung; Lu, Cheng Nan; Jawan, Bruno; Wang, Cheng Haung.

In: Biochemical and Biophysical Research Communications, Vol. 336, No. 1, 14.10.2005, p. 324-331.

Research output: Contribution to journalArticle

Hung, Kung Sheng ; Lee, Tsung Hsing ; Chou, Wen Ying ; Wu, Chia Ling ; Cho, Chung Lung ; Lu, Cheng Nan ; Jawan, Bruno ; Wang, Cheng Haung. / Interleukin-10 gene therapy reverses thioacetamide-induced liver fibrosis in mice. In: Biochemical and Biophysical Research Communications. 2005 ; Vol. 336, No. 1. pp. 324-331.
@article{06eb8a3c93274663983ec759a53f259d,
title = "Interleukin-10 gene therapy reverses thioacetamide-induced liver fibrosis in mice",
abstract = "Hepatic fibrosis represents a process of healing and scarring in response to chronic liver injury. Interleukin-10 (IL-10) is a cytokine that downregulates the proinflammatory response and has a modulatory effect on hepatic fibrogenesis. The aim of this study was to investigate whether IL-10 gene therapy possesses anti-hepatic fibrogenesis in mice. Liver fibrosis was induced by long-term thioacetamide administration in mice. Human IL-10 expression plasmid was delivered via electroporation after liver fibrosis established. IL-10 gene therapy reversed hepatic fibrosis and prevented cell apoptosis in a thioacetamide-treated liver. RT-PCR revealed IL-10 gene therapy to reduce liver transforming growth factor-β1, tumor necrosis factor-α, collagen α1, cell adhesion molecule, and tissue inhibitors of metalloproteinase mRNA upregulation. Following gene transfer, the activation of α-smooth muscle actin and cyclooxygenase-2 was significantly attenuated. In brief, IL-10 gene therapy might be an effective therapeutic reagent for liver fibrosis with potential future clinical applications.",
keywords = "COX-2, Gene therapy, IL-10, Liver fibrosis, Thioacetamide",
author = "Hung, {Kung Sheng} and Lee, {Tsung Hsing} and Chou, {Wen Ying} and Wu, {Chia Ling} and Cho, {Chung Lung} and Lu, {Cheng Nan} and Bruno Jawan and Wang, {Cheng Haung}",
year = "2005",
month = "10",
day = "14",
doi = "10.1016/j.bbrc.2005.08.085",
language = "English",
volume = "336",
pages = "324--331",
journal = "Biochemical and Biophysical Research Communications",
issn = "0006-291X",
publisher = "Elsevier B.V.",
number = "1",

}

TY - JOUR

T1 - Interleukin-10 gene therapy reverses thioacetamide-induced liver fibrosis in mice

AU - Hung, Kung Sheng

AU - Lee, Tsung Hsing

AU - Chou, Wen Ying

AU - Wu, Chia Ling

AU - Cho, Chung Lung

AU - Lu, Cheng Nan

AU - Jawan, Bruno

AU - Wang, Cheng Haung

PY - 2005/10/14

Y1 - 2005/10/14

N2 - Hepatic fibrosis represents a process of healing and scarring in response to chronic liver injury. Interleukin-10 (IL-10) is a cytokine that downregulates the proinflammatory response and has a modulatory effect on hepatic fibrogenesis. The aim of this study was to investigate whether IL-10 gene therapy possesses anti-hepatic fibrogenesis in mice. Liver fibrosis was induced by long-term thioacetamide administration in mice. Human IL-10 expression plasmid was delivered via electroporation after liver fibrosis established. IL-10 gene therapy reversed hepatic fibrosis and prevented cell apoptosis in a thioacetamide-treated liver. RT-PCR revealed IL-10 gene therapy to reduce liver transforming growth factor-β1, tumor necrosis factor-α, collagen α1, cell adhesion molecule, and tissue inhibitors of metalloproteinase mRNA upregulation. Following gene transfer, the activation of α-smooth muscle actin and cyclooxygenase-2 was significantly attenuated. In brief, IL-10 gene therapy might be an effective therapeutic reagent for liver fibrosis with potential future clinical applications.

AB - Hepatic fibrosis represents a process of healing and scarring in response to chronic liver injury. Interleukin-10 (IL-10) is a cytokine that downregulates the proinflammatory response and has a modulatory effect on hepatic fibrogenesis. The aim of this study was to investigate whether IL-10 gene therapy possesses anti-hepatic fibrogenesis in mice. Liver fibrosis was induced by long-term thioacetamide administration in mice. Human IL-10 expression plasmid was delivered via electroporation after liver fibrosis established. IL-10 gene therapy reversed hepatic fibrosis and prevented cell apoptosis in a thioacetamide-treated liver. RT-PCR revealed IL-10 gene therapy to reduce liver transforming growth factor-β1, tumor necrosis factor-α, collagen α1, cell adhesion molecule, and tissue inhibitors of metalloproteinase mRNA upregulation. Following gene transfer, the activation of α-smooth muscle actin and cyclooxygenase-2 was significantly attenuated. In brief, IL-10 gene therapy might be an effective therapeutic reagent for liver fibrosis with potential future clinical applications.

KW - COX-2

KW - Gene therapy

KW - IL-10

KW - Liver fibrosis

KW - Thioacetamide

UR - http://www.scopus.com/inward/record.url?scp=24344439724&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=24344439724&partnerID=8YFLogxK

U2 - 10.1016/j.bbrc.2005.08.085

DO - 10.1016/j.bbrc.2005.08.085

M3 - Article

C2 - 16126171

AN - SCOPUS:24344439724

VL - 336

SP - 324

EP - 331

JO - Biochemical and Biophysical Research Communications

JF - Biochemical and Biophysical Research Communications

SN - 0006-291X

IS - 1

ER -