Curcumin suppresses the expression of extracellular matrix genes in activated hepatic stellate cells by inhibiting gene expression of connective tissue growth factor

Zheng, Shizhong; Chen, Anping

doi:10.1152/ajpgi.00450.2005

Cited by 82 publications

(79 citation statements)

References 56 publications

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“…24 Our recent results supported the proposal and demonstrated an antagonistic relationship between the activation of TGF-b signaling and the gene expression of PPARg in HSC. 24 The attention of the current study was paid to the role of PDGF and/or EGF signaling in the curcumin induction of PPARg gene expression in activated HSC. Results in this report demonstrated that exogenous PDGF or EGF caused a dosedependent reduction in PPARg gene expression in passaged HSC (Figure 1).…”

Section: Activating Pdgf and Egf Signaling Inhibits Pparc Expression supporting

confidence: 85%

“…Cells were serum-starved in DMEM for 48 h, which made cells more sensitive to serum stimulation. [22][23][24] Serum-starved cells were pretreated with curcumin for 30 min before the stimulation with FBS (10%) for an additional 20 min. Whole-cell extracts were prepared.…”

Section: Curcumin Reduces Tyrosine Phosphorylation Of Pdgf-br and Egfrmentioning

confidence: 99%

“…Prior experiments suggested that 10% of FBS might contain enough agonists to activate PPARg in HSC. 11,[22][23][24] The induction of PPARg expression resulted in the stimulation of its activity in cultured HSC. [22][23][24] It is of interest to evaluate the role of PI-3K/AKT, ERK, and JNK activity in the curcumin induction of gene expression of PPARg.…”

Section: Curcumin Reduces Tyrosine Phosphorylation Of Pdgf-br and Egfrmentioning

confidence: 99%

“…9 We previously demonstrated that curcumin inhibited cell proliferation and induced apoptosis of activated HSC. [22][23][24] The underlying mechanisms remain largely to be defined. The signaling pathways of PI-3K/AKT, ERK and JNK are critically relevant to cell proliferation and cell survival in many cell types, including in HSC.…”

Section: Activating Pdgf and Egf Signaling Inhibits Pparc Expression mentioning

confidence: 99%

“…21 We recently reported that curcumin induced gene expression of endogenous PPARg in activated HSC in vitro, which was a prerequisite in the curcumin inhibition of HSC growth, induction of apoptosis and suppression of extracellular matrix gene expression. [22][23][24] The aim of this study is to elucidate the mechanisms of curcumin in the induction of PPARg gene expression in activated HSC, focusing on the impact of PDGF and EGF signaling. It is hypothesized that the interruption of the PDGF and EGF signaling pathways by curcumin might stimulate gene expression of PPARg in activated HSC.…”

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The interruption of the PDGF and EGF signaling pathways by curcumin stimulates gene expression of PPARγ in rat activated hepatic stellate cell in vitro

Zhou

Zheng

Lin

et al. 2007

Laboratory Investigation

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Activation of hepatic stellate cells (HSC), the major effector in hepatic fibrogenesis, is coupled with sequential alterations in expression of genes, including the upregulation of platelet-derived growth factor-b receptor (PDGF-bR) and epidermal growth factor receptor (EGFR), as well as the down-regulation of the peroxisome proliferator-activated receptor-g (PPARg). However, the relationship among the alterations in expression of the genes and the activation of their signaling in activated HSC remains obscure. We recently showed that curcumin, the yellow pigment in curry, inhibited cell growth and induced gene expression of endogenous PPARg in activated HSC in vitro. The present study is to elucidate the underlying mechanisms, focusing on the impacts of PDGF and EGF signaling. It is hypothesized that the interruption of the PDGF and EGF signaling pathways by curcumin might stimulate gene expression of PPARg in activated HSC. Our results in this report indicate that the activation of PDGF or EGF signaling by exogenous PDGF or EGF inhibits PPARg gene expression in passaged HSC. Curcumin interrupts PDGF and EGF signaling demonstrated by inhibiting tyrosine phosphorylation of PDGF-bR and EGFR and by reducing the levels of phosphorylated phosphatidylinositol-3 kinase (PI-3K/ AKT), extracellular signal-regulated kinase (ERK) and the Jun N-terminal kinase (JNK). The blockade of PI-3K/AKT, ERK or JNK signaling negatively regulates PPARg gene expression in activated HSC, leading to the reduction in cell growth, including inducing cell arrest and apoptosis. Our results collectively demonstrate that the interruption of the PDGF and EGF signaling pathways by curcumin stimulates gene expression of PPARg in activated HSC. These results provide novel insights into the mechanisms of curcumin in the induction of PPARg gene expression in activated HSC.

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Section: Activating Pdgf and Egf Signaling Inhibits Pparc Expression supporting

confidence: 85%

Section: Curcumin Reduces Tyrosine Phosphorylation Of Pdgf-br and Egfrmentioning

confidence: 99%

Section: Curcumin Reduces Tyrosine Phosphorylation Of Pdgf-br and Egfrmentioning

confidence: 99%

Section: Activating Pdgf and Egf Signaling Inhibits Pparc Expression mentioning

confidence: 99%

mentioning

confidence: 99%

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The interruption of the PDGF and EGF signaling pathways by curcumin stimulates gene expression of PPARγ in rat activated hepatic stellate cell in vitro

Zhou

Zheng

Lin

et al. 2007

Laboratory Investigation

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Hepatic Stellate Cells

Rojkind

Reyes‐Gordillo

2009

The Liver

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Why it is necessary to translate curcumin into clinical practice for the prevention and treatment of metabolic syndrome?

Sahebkar

2012

BioFactors

145

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Curcumin (diferuloylmethane) is the yellow-orange pigment of dried Curcuma longa L. rhizomes (turmeric). During the past two decades, there has been a large volume of published studies describing the biological and pharmacological properties of this phytochemical including anticancer, anti-inflammatory, antioxidant, antithrombotic, antiatherosclerotic, cardioprotective, neuroprotective, memory enhancing, antiparkinsonism, antirheumatic, anti-infectious, antiaging, antipsoriatic, and anticonvulsant activities. In addition, curcumin has been shown to be extremely safe and interact with multiple molecular targets that are involved in the pathogenesis of metabolic syndrome. Curcumin could favorably affect all leading components of metabolic syndrome including insulin resistance, obesity, hypertriglyceridemia, decreased HDL-C and hypertension, and prevent the deleterious complications of MetS including diabetes and cardiovascular disease. Owing to its antioxidant and anti-inflammatory properties, curcumin can also exert several pleiotropic effects and improve endothelial dysfunction, adipokine imbalances, and hyperuricemia which usually accompany MetS. Despite the potential tremendous benefit of this multifaceted phytopharmaceutical, no trial result has yet been publicized on this issue. This review seeks to briefly summarize the ample scientific evidence that supports the therapeutic efficacy of curcumin, at least as an adjunctive treatment, in patients with MetS.

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Curcumin suppresses the expression of extracellular matrix genes in activated hepatic stellate cells by inhibiting gene expression of connective tissue growth factor

Abstract: Zheng, Shizhong, and Anping Chen. Curcumin suppresses the expression of extracellular matrix genes in activated hepatic stellate cells by inhibiting gene expression of connective tissue growth factor.

Cited by 82 publications

References 56 publications

The interruption of the PDGF and EGF signaling pathways by curcumin stimulates gene expression of PPARγ in rat activated hepatic stellate cell in vitro

The interruption of the PDGF and EGF signaling pathways by curcumin stimulates gene expression of PPARγ in rat activated hepatic stellate cell in vitro

Hepatic Stellate Cells

Why it is necessary to translate curcumin into clinical practice for the prevention and treatment of metabolic syndrome?

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