Extracellular signal-regulated kinase activation differentially regulates platelet-derived growth factor's actions in hepatic stellate cells, and is induced by In Vivo liver injury in the rat

Marra, Fabio; Arrighi, Maria Cristina; Fazi, Marilena; Caligiuri, Alessandra; Pinzani, Massimo; Romanelli, Roberto Giulio; Efsen, Eva; Laffi, Giacomo; Geñtilini, Paolo

doi:10.1002/hep.510300406

Cited by 160 publications

(120 citation statements)

References 52 publications

(75 reference statements)

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“…7A and B). HSC lysates from CCl 4 -injured livers, in which activation of ERK1/2 was already reported [22], were characterized by a very significant increase of JNK activity (24 h) and (6 h) heme oxygenase 1 (HO-1), a cytoprotective enzyme that is considered a marker of ongoing oxidative stress ( Fig. 7 C and D).…”

Section: Increased Generation Of Ros and Jnk Activity In Vivomentioning

confidence: 57%

Intracellular reactive oxygen species are required for directional migration of resident and bone marrow-derived hepatic pro-fibrogenic cells

Novo

Busletta

Bonzo

et al. 2011

Journal of Hepatology

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111

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Section: Increased Generation Of Ros and Jnk Activity In Vivomentioning

confidence: 57%

Intracellular reactive oxygen species are required for directional migration of resident and bone marrow-derived hepatic pro-fibrogenic cells

Novo

Busletta

Bonzo

et al. 2011

Journal of Hepatology

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111

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“…Preincubation with canrenone did not affect early signaling events, including PDGF-␤ receptor phosphorylation or the phosphorylation of PLC-␥, a molecule physically associated with the PDGF receptor. Although the activation of ERK has been shown to be necessary for the mitogenic effect of PDGF, 28,47 the inhibitory effect of canrenone on PDGF-induced mitogenesis and chemotaxis is not exerted through an interference with the activity of this kinase, as also confirmed by the absence of inhibition of its downstream nuclear target c-fos. However, data presented herein indicate that canrenone dosedependently reduces PDGF-induced activity of PI 3-K, a lipid and protein kinase activated through several different pathways, which has been shown to be necessary for both mitogenesis and chemotaxis induced by PDGF in HSC.…”

Section: Discussionmentioning

confidence: 97%

Antifibrogenic effects of canrenone, an antialdosteronic drug, on human hepatic stellate cells

et al. 2003

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“…36 In hepatocytes, activation of ERK results in stimulation of DNA synthesis. 37 The AKT/PKB pathway is an important antiapoptotic factor in hepatocytes and exerts protective effects against cell death. 38 Interestingly, AKT-driven cell signaling is altered by CS in other organs.…”

Section: Discussionmentioning

confidence: 99%

Cigarette Smoking Exacerbates Nonalcoholic Fatty Liver Disease in Obese Rats

et al. 2010

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The prevalence of cigarette smoking (CS) is increased among obese subjects, who are susceptible to develop nonalcoholic fatty liver disease (NAFLD). We investigated the hepatic effects of CS in control and obese rats. Control and obese Zucker rats were divided into smokers and nonsmokers (n ‫؍‬ 12 per group). Smoker rats were exposed to 2 cigarettes/day, 5 days/week for 4 weeks. The effects of CS were assessed by biochemical analysis, hepatic histological examination, immunohistochemistry, and gene expression analysis. Phosphorylation of AKT and extracellular signal-regulated kinase (ERK) and quantification of carbonylated proteins were assessed by western blotting. As expected, obese rats showed hypercholesterolemia, insulin resistance, and histological features of NAFLD. Smoking did not modify the lipidic or glucidic serum profiles. Smoking increased alanine aminotransferase serum levels and the degree of liver injury in obese rats, whereas it only induced minor changes in control rats. Importantly, CS increased the histological severity of NAFLD in obese rats. We also explored the potential mechanisms involved in the deleterious effects of CS. Smoking increased the degree of oxidative stress and hepatocellular apoptosis in obese rats, but not in controls. Similarly, smoking increased the hepatic expression of tissue inhibitor of metalloproteinase-1 and procollagen-alpha2(I) in obese rats, but not in controls. C igarette smoking (CS) is considered a worldwide major cause of preventable morbidity and mortality. 1 The main clinical consequences of prolonged exposure to CS are chronic respiratory diseases, increased incidence of a variety of cancers, and increased risk of atherothrombotic clinical events such as myocardial infarction. 2 Hepatologists have traditionally paid scant attention to the deleterious effects of CS. This reflects the fact that smoking per se does not appear to cause liver injury and therefore is not considered a causative agent for chronic liver diseases. 3 However, there is in-

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Extracellular signal-regulated kinase activation differentially regulates platelet-derived growth factor's actions in hepatic stellate cells, and is induced by In Vivo liver injury in the rat

Cited by 160 publications

References 52 publications

Intracellular reactive oxygen species are required for directional migration of resident and bone marrow-derived hepatic pro-fibrogenic cells

Intracellular reactive oxygen species are required for directional migration of resident and bone marrow-derived hepatic pro-fibrogenic cells

Antifibrogenic effects of canrenone, an antialdosteronic drug, on human hepatic stellate cells

Cigarette Smoking Exacerbates Nonalcoholic Fatty Liver Disease in Obese Rats

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