Caveolin-1 is upregulated in hepatic stellate cells but not sinusoidal endothelial cells after liver injury. Issue 2 (April 2016)

• Record Type: Journal Article
• Authors: Singh, Shweta; Liu, Songling; Rockey, Don C.
• Is Part Of: Tissue & cell. Volume 48:Issue 2(2016)
• Page Start: 126
• Page End: 132
• Publication Date: 2016-04
• Subjects: Nitric oxide -- eNOS -- Signaling -- Immunohistochemistry -- Immunoblotting; Cytology -- Periodicals; 571.5
• DOI: 10.1016/j.tice.2015.12.006
• Languages: English
• ISSNs: 0040-8166

Abstract

Graphical abstract: Immunohistochemical detection of caveolin-1 in normal and injured rat liver tissue. The images depict caveolin-1 co-labeling with desmin (a marker of HSCs), which is greater in the injured liver than the normal liver. Desmin labeling is visualized in portal and central vascular structures, in addition to HSCs. Highlights: Caveolin-1 is upregulated after liver injury. The only cell compartment in which caveolin-1 is upregulated is the HSC. Since caveolin-1 is an important signaling molecule, the findings have functional implications in the injured rat liver. Abstract: Sinusoidal endothelial cells (SEC) and hepatic stellate cells (HSC) are closely associated specialized vascular cells residing in the hepatic sinusoid. These cells have been shown to play important roles in many different pathophysiologic processes, in particular in liver fibrosis/cirrhosis and portal hypertension. Caveolin-1 functions as a scaffolding protein, and has a variety of functions including in many disease states, such as liver cirrhosis. Although previous studies have shown that in the injured rat liver, caveolin-1 is upregulated, the precise cells in which remains unclear. Therefore, the purpose of this study was to clarify the cell type (or types) in which caveolin-1 is expressed in normal and injured rat liver. We have utilized both detailed immunohistochemical labeling with cell specific markers as well as cell isolation techniques (isolating sinusoidal endothelial cells, HSCs, and hepatocytes) in normal and injured (bile duct ligation) rat liver. We show here that in the normal liver caveolin-1 is expressed predominantly in HSCs and SECs but after liver injury there is upregulation of caveolin-1 in HSCs, but not in SECs. These data have functional implications for the cells in which caveolin-1 is regulated.