Abstract

Sinusoidal endothelial cells and hepatocytes increase in number after partial resection and necrosis of the liver, and contribute to both reconstruction and capillarization of the sinusoids through interaction with stellate cells. The mechanism underlying such interaction was evaluated regarding angiopoietins and tie receptors essential for blood vessel formation. Hepatic mRNA expressions of angiopoietin-1, angiopoietin-2 and tie-2 were increased at 168 h after 70% liver resection with sinusoidal reconstruction in rats, and also at 48 h with sinusoidal capillarization in the liver of rats given carbon tetrachloride (CCl4). Tie-2 mRNA expression was detected in sinusoidal endothelial cells and stellate cells isolated from normal rats, and in activated stellate cells from CCl4-intoxicated rats. The mRNA expressions of angiopoietin-1 and angiopoietin-2 were detectable in Kupffer cells, sinusoidal endothelial cells and stellate cells in normal rats, but increased in activated stellate cells and macrophages after CCl4-intoxication. Both angiopoietins and tie-2 were immunohistochemically stained along the sinusoids of 70% hepatectomized rats and in necrotic areas of CCl4-intoxicated rats. Angiopoietin-1 and angiopoietin-2 may be involved in both reconstruction and capillarization of the sinusoids in rat liver after partial resection and necrosis through interaction between stellate cells and sinusoidal and vascular endothelial cells via tie-2 receptor.

Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.