Literature DB >> 23515440

A synthetic PPAR-γ agonist triterpenoid ameliorates experimental fibrosis: PPAR-γ-independent suppression of fibrotic responses.

Jun Wei1, Hongyan Zhu, Kazuhiro Komura, Gabriel Lord, Michal Tomcik, Wenxia Wang, Sruthi Doniparthi, Zenshiro Tamaki, Monique Hinchcliff, Joerg H W Distler, John Varga.   

Abstract

BACKGROUND: Persistent fibroblast activation initiated by transforming growth factor β (TGF-β) is a fundamental event in the pathogenesis of systemic sclerosis, and its pharmacological inhibition represents a potential therapeutic strategy. The nuclear receptor, peroxisome proliferator-activated receptor γ (PPAR-γ), exerts potent fibrotic activity. The synthetic oleanane triterpenoid, 2-cyano-3,12-dioxo-olean-1,9-dien-28-oic acid (CDDO), is a PPAR-γ agonist with potential effects on TGF-β signalling and dermal fibrosis.
OBJECTIVE: To examine the modulation of fibrogenesis by CDDO in explanted fibroblasts, skin organ cultures and murine models of scleroderma.
MATERIAL AND METHODS: The effects of CDDO on experimental fibrosis induced by bleomycin injection or by overexpression of constitutively active type I TGF-β receptor (TgfbR1ca) were evaluated. Modulation of fibrotic gene expression was examined in human skin organ cultures. To delineate the mechanisms underlying the antifibrotic effects of CDDO, explanted skin fibroblasts cultured in two-dimensional monolayers or in three-dimensional full-thickness human skin equivalents were studied.
RESULTS: CDDO significantly ameliorated dermal fibrosis in two complementary mouse models of scleroderma, as well as in human skin organ cultures and in three-dimensional human skin equivalents. In two-dimensional monolayer cultures of explanted normal fibroblasts, CDDO abrogated fibrogenic responses induced by TGF-β. These CDDO effects occurred via disruption of Smad-dependent transcription and were associated with inhibition of Akt activation. In scleroderma fibroblasts, CDDO attenuated the elevated synthesis of collagen. Remarkably, the in vitro antifibrotic effects of CDDO were independent of PPAR-γ.
CONCLUSIONS: The PPAR-γ agonist triterpenoid CDDO attenuates fibrogenesis by antagonistically targeting canonical TGF-β/Smad and Akt signalling in a PPAR-γ-independent manner. These findings identify this synthetic triterpenoid as a potential new therapy for the control of fibrosis.

Entities:  

Keywords:  CDDO; PPAR-γ; TGF-β; fibroblast; fibrosis; murine scleroderma; triterpenoid

Mesh:

Substances:

Year:  2013        PMID: 23515440      PMCID: PMC4028127          DOI: 10.1136/annrheumdis-2012-202716

Source DB:  PubMed          Journal:  Ann Rheum Dis        ISSN: 0003-4967            Impact factor:   19.103


  55 in total

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2.  Regulation of peroxisome proliferator-activated receptor-gamma in liver fibrosis.

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Journal:  Am J Physiol Gastrointest Liver Physiol       Date:  2006-06-22       Impact factor: 4.052

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7.  Loss of peroxisome proliferator-activated receptor gamma in mouse fibroblasts results in increased susceptibility to bleomycin-induced skin fibrosis.

Authors:  Mohit Kapoor; Matthew McCann; Shangxi Liu; Kun Huh; Christopher P Denton; David J Abraham; Andrew Leask
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  34 in total

Review 1.  Fibrosis--a lethal component of systemic sclerosis.

Authors:  Yuen Yee Ho; David Lagares; Andrew M Tager; Mohit Kapoor
Journal:  Nat Rev Rheumatol       Date:  2014-04-22       Impact factor: 20.543

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Authors:  Lara Bossini-Castillo; Elena López-Isac; Maureen D Mayes; Javier Martín
Journal:  Semin Immunopathol       Date:  2015-06-02       Impact factor: 9.623

3.  Peroxisome proliferator-activated receptor-γ agonist troglitazone suppresses transforming growth factor-β1 signalling through miR-92b upregulation-inhibited Axl expression in human keloid fibroblasts in vitro.

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5.  The Histone Deacetylase Sirtuin 1 Is Reduced in Systemic Sclerosis and Abrogates Fibrotic Responses by Targeting Transforming Growth Factor β Signaling.

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Review 6.  Evolving insights into the cellular and molecular pathogenesis of fibrosis in systemic sclerosis.

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7.  Nrf2 exerts cell-autonomous antifibrotic effects: compromised function in systemic sclerosis and therapeutic rescue with a novel heterocyclic chalcone derivative.

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Review 9.  Therapeutic targets for treating fibrotic kidney diseases.

Authors:  So-Young Lee; Sung I Kim; Mary E Choi
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10.  Scleroderma keratinocytes promote fibroblast activation independent of transforming growth factor beta.

Authors:  Sara S McCoy; Tamra J Reed; Celine C Berthier; Pei-Suen Tsou; Jianhua Liu; Johann E Gudjonsson; Dinesh Khanna; J Michelle Kahlenberg
Journal:  Rheumatology (Oxford)       Date:  2017-11-01       Impact factor: 7.580

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