Induction of beta-platelet-derived growth factor receptor in rat hepatic lipocytes during cellular activation in vivo and in culture.

Wong, Lu-Min; Yamasaki, Glenn; Johnson, Richard J.; Friedman, Scott L.

doi:10.1172/jci117497

Cited by 285 publications

(208 citation statements)

References 40 publications

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“…These changes include the expression of new receptors, such as platelet-derived growth factor  receptors 1 and 2. Other receptors, such as the receptor for insulin-like growth factor 1 and endothelin are present on both quiescent and activated HSCs [4,5]. Several soluble factors, including growth factors, cytokines, chemokines and oxidative stress products, play a role in the activation of HSCs.…”

Section: Introductionmentioning

confidence: 99%

Zinc supplementation attenuates ethanol- and acetaldehyde-induced liver stellate cell activation by inhibiting reactive oxygen species (ROS) production and by influencing intracellular signaling

Szuster‐Ciesielska

Plewka

Daniluk

et al. 2009

Biochemical Pharmacology

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To cite this version:Agnieszka Szuster-Ciesielska, Krzysztof Plewka, Jadwiga Daniluk, Martyna Kandefer-Szerszeń. Zinc supplementation attenuates ethanol-and acetaldehyde-induced liver stellate cell activation by inhibiting reactive oxygen species (ROS) production and by influencing intracellular signaling. Biochemical Pharmacology, Elsevier, 2009, 78 (3) This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.

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Section: Introductionmentioning

confidence: 99%

Zinc supplementation attenuates ethanol- and acetaldehyde-induced liver stellate cell activation by inhibiting reactive oxygen species (ROS) production and by influencing intracellular signaling

Szuster‐Ciesielska

Plewka

Daniluk

et al. 2009

Biochemical Pharmacology

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“…PDGF is the most potent proliferating stimulus for HSCs (4,8). It has been reported that the PDGF receptor (PDGFR) is up-regulated along with HSC activation in carbon tetrachloride (CCl4)-and bile duct ligation-induced liver injuries (9)(10)(11). Dominant-negative soluble PDGFR or anti-sense PDGF gene transfer significantly attenuated experimental liver fibrosis development (12,13).…”

Section: Introductionmentioning

confidence: 99%

Amelioration of liver fibrogenesis by dual inhibition of PDGF and TGF-β with a combination of imatinib mesylate and ACE inhibitor in rats

Yoshiji¹,

Kuriyama²,

Noguchi³

et al. 2006

Int J Mol Med

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Abstract. Both platelet-derived growth factor (PDGF) and transforming growth factor-ß (TGF-ß) are known to be pivotal cytokines in liver fibrosis development. The aim of our current study was to elucidate the effects of dual inhibition of PDGF and TGF-ß by combination of the clinically used imatinib mesylate (STI-571) and perindopril (an ACEinhibitor; ACE-I), respectively, on ongoing liver fibrosis development in rats. The effects of STI-571 and ACE-I at clinically comparable low doses were examined in a rat model of CCl4-induced liver fibrogenesis. Treatment with both STI-571 and ACE-I inhibited liver fibrogenesis and suppressed activation of hepatic stellate cells (HSCs). Administration of both agents exerted a more potent inhibitory effect than administration of either single agent. Our in vitro study demonstrated that STI-571 and ACE-I suppressed PDGF receptor (PDGFR) phosphorylation and TGF-ß expression in activated HSCs, respectively. Dual suppression of PDGF and TGF-ß with a combination of clinically comparable low doses of STI-571 and ACE-I exerted a significant inhibitory effect on ongoing liver fibrosis development. Since both agents are widely used in clinical practice, this combination therapy may provide a new strategy against liver fibrosis in the future.

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“…2,3 Induction of PDGF-B and PDGFRb in HSC is well documented in single-dose carbon tetrachloride (CCl 4 )-induced acute liver injury and during early stages of bile duct ligation (BDL). 4,5 Of the newly discovered isoforms, PDGF-C and -D, only PDGF-D showed significant upregulation in the BDL rat model. 3 Previous experiments using the CCl 4 model were confined to a period of 1-2 weeks and mainly represented single-dose CCl 4 applications.…”

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confidence: 99%

Platelet-derived growth factor isoform expression in carbon tetrachloride-induced chronic liver injury

Borkham-Kamphorst

Коваленко

Roeyen

et al. 2008

Laboratory Investigation

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Platelet-derived growth factor (PDGF) has an essential role in liver fibrogenesis, as PDGF-B and -D both act as potent mitogens on culture-activated hepatic stellate cells (HSCs). Induction of PDGF receptor type-b (PDGFRb) in HSC is well documented in single-dose carbon tetrachloride (CCl 4 )-induced acute liver injury. Of the newly discovered isoforms PDGF-C and -D, only PDGF-D shows significant upregulation in bile duct ligation (BDL) models. We have now investigated the expression of PDGF isoforms and receptors in chronic liver injury in vivo after long-term CCl 4 treatment and demonstrated that isolated hepatocytes have the requisite PDGF signaling pathways, both in the naive state and when isolated from CCl 4 -treated rats. In vivo, PDGF gene expression showed upregulation of all PDGF isoforms and receptors, with values peaking at 4 weeks and decreasing to near basal levels by 8 and 12 weeks. Interestingly, PDGF-C increased significantly when compared to BDL-models. PDGF-A, PDGF-C and PDGF receptor type-a (PDGFRa) correlated closely with inflammation and steatosis. Immunohistochemistry revealed expression of PDGF-B, -C and -D in areas corresponding to centrilobular necrosis, inflammation and fibrosis, whereas PDGF-A localized in regenerative hepatocytes. PDGFRb was identified along the fibrotic septa, whereas PDGFRa showed positive staining in fibrotic septa and regenerative hepatocytes. Despite a significant decline of PDGF isoforms, hepatocyte regeneration peaked at 8 weeks. A marked difference in the degree of fibrosis was observed amongst the individual animals. In summary, PDGF expression in liver damage primarily parallels mesenchymal cell proliferation and extracellular matrix production, rather than hepatocyte regeneration. We conclude that PDGF levels in chronic liver injury peak at 4 weeks after onset of injury, and that the outcome of chronic toxic liver injury strongly depends on the individual capacity for tissue regeneration in the weeks following the peak of PDGF expression.

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Induction of beta-platelet-derived growth factor receptor in rat hepatic lipocytes during cellular activation in vivo and in culture.

Abstract: Invest. 1994Invest. . 94:1563Invest. -1569

Cited by 285 publications

References 40 publications

Zinc supplementation attenuates ethanol- and acetaldehyde-induced liver stellate cell activation by inhibiting reactive oxygen species (ROS) production and by influencing intracellular signaling

Zinc supplementation attenuates ethanol- and acetaldehyde-induced liver stellate cell activation by inhibiting reactive oxygen species (ROS) production and by influencing intracellular signaling

Amelioration of liver fibrogenesis by dual inhibition of PDGF and TGF-β with a combination of imatinib mesylate and ACE inhibitor in rats

Platelet-derived growth factor isoform expression in carbon tetrachloride-induced chronic liver injury

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