2009, English, Article edition: Growth arrest-specific protein 6 deficiency impairs liver tissue repair after acute toxic hepatitis in mice. Lafdil, Fouad; Chobert, Marie-Noële; Deveaux, Vanessa; ...

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Physical Description
  • text
Published
  • HAL - CCSD
  • 2009
Language
  • English

Edition details

Title
  • Growth arrest-specific protein 6 deficiency impairs liver tissue repair after acute toxic hepatitis in mice.
Author
  • Lafdil, Fouad
  • Chobert, Marie-Noële
  • Deveaux, Vanessa
  • Zafrani, Elie-Serge
  • Mavier, Philippe
  • Nakano, Toru
  • Laperche, Yannick
  • Brouillet, Arthur
Published
  • HAL - CCSD
  • 2009
Physical Description
  • text
Subjects
Notes
  • BACKGROUND/​AIMS: Resident macrophages and myofibroblasts derived from hepatic stellate cells play a key role in liver wound healing. We previously reported that these sinusoidal cells secrete the growth arrest-specific protein 6 (Gas6) and express Axl, one of its receptors. Here we address the role of Gas6 in the healing process during acute liver injury. METHODS: Toxic hepatitis was induced by a single carbon tetrachloride injection in Gas6 deficient (Gas6(-/​-)) mice and liver recovery was compared with wild-type animals. RESULTS: Gas6 deficiency did not cause any change in CCl(4)-induced liver damage. At 72 h, an efficient tissue repair was observed in wild-type animals whereas in Gas6(-/​-) mice, we noticed a defective wound healing accounted by reduced Kupffer cell activation revealed by a decrease in the induction of CD14, TNF-alpha, IL6 and MCP-1. Gas6-deficiency, by limiting cytokine/​chemokine release, prevents hepatocyte proliferation, recruitment of circulating monocytes and accumulation of myofibroblasts in healing areas. We also report a direct chemotactic effect of Gas6 on circulating monocytes which might explain defective macrophage infiltration in liver necrotic areas of Gas6(-/​-) mice. Interestingly in Gas6(-/​-) mice, we observed a high and constitutive expression of Axl and an induction of the suppressor of cytokine signaling SOCS1 after CCl(4) treatment. CONCLUSIONS: The lower level of cytokines/​chemokines in Gas6(-/​-) mice after CCl(4) injury, is the consequence of an inhibitory signal arising from Axl receptor overexpression, leading to delayed liver repair in deficient mice.
  • HAL:inserm-00405375, version 1
  • HAL:http:/​/​www.hal.inserm.fr/​inserm-00405375/​en/​
  • PUBMED:19443073
  • DOI:10.1016/​j.jhep.2009.02.030
Language
  • English
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