Endothelial cells are damaged by autophagic induction before hepatocytes in Con A-induced acute hepatitis

Ming Chen Yang, Chih Peng Chang, Huan Yao Lei

Research output: Contribution to journalArticle

20 Citations (Scopus)

Abstract

We have reported both T-cell-dependent and -independent hepatitis in immunocompetent and immunodeficiency mice, respectively, after intravenous injection of Con A in mice. The mode of hepatocyte cell death is different: autophagy for T-cell-independent hepatitis in contrast to apoptosis for T-cell-dependent one. In this study, we further demonstrate that liver blood vessels are the first target in both modes. The infused Con A bond to the hepatic vascular endothelial cells and cause its damage with autophagy. Before the elevation of the serum alanine aminotransferase at 6 h post-injection, the plasma leakage and hemorrhage occur at 1-3 h without inflammation. Con A induces autophagy of endothelial cells and hemorrhage that is enhanced by IFN-γ. Using the endothelial cell line HMEC-1, a dose-and time-dependent cell death with autophagic LC3-II (microtubule-associated protein light chain 3) conversion was induced by Con A and was enhanced by IFN-γ. In conclusion, Con A induced autophagy on hepatic endothelial cells; the damage of liver blood vessel occurs before the induction of T-cell-dependent hepatitis via apoptosis or T-cell-independent hepatitis via autophagy.

Original languageEnglish
Pages (from-to)661-670
Number of pages10
JournalInternational Immunology
Volume22
Issue number8
DOIs
Publication statusPublished - 2010 Jun 13

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Autophagy
Hepatitis
Hepatocytes
Endothelial Cells
T-Lymphocytes
Blood Vessels
Liver
Apoptosis
Hemorrhage
Microtubule-Associated Proteins
Alanine Transaminase
Intravenous Injections
Cell Death
Inflammation
Light
Cell Line
Injections
Serum

All Science Journal Classification (ASJC) codes

  • Immunology and Allergy
  • Immunology

Cite this

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abstract = "We have reported both T-cell-dependent and -independent hepatitis in immunocompetent and immunodeficiency mice, respectively, after intravenous injection of Con A in mice. The mode of hepatocyte cell death is different: autophagy for T-cell-independent hepatitis in contrast to apoptosis for T-cell-dependent one. In this study, we further demonstrate that liver blood vessels are the first target in both modes. The infused Con A bond to the hepatic vascular endothelial cells and cause its damage with autophagy. Before the elevation of the serum alanine aminotransferase at 6 h post-injection, the plasma leakage and hemorrhage occur at 1-3 h without inflammation. Con A induces autophagy of endothelial cells and hemorrhage that is enhanced by IFN-γ. Using the endothelial cell line HMEC-1, a dose-and time-dependent cell death with autophagic LC3-II (microtubule-associated protein light chain 3) conversion was induced by Con A and was enhanced by IFN-γ. In conclusion, Con A induced autophagy on hepatic endothelial cells; the damage of liver blood vessel occurs before the induction of T-cell-dependent hepatitis via apoptosis or T-cell-independent hepatitis via autophagy.",
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Endothelial cells are damaged by autophagic induction before hepatocytes in Con A-induced acute hepatitis. / Yang, Ming Chen; Chang, Chih Peng; Lei, Huan Yao.

In: International Immunology, Vol. 22, No. 8, 13.06.2010, p. 661-670.

Research output: Contribution to journalArticle

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