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IL-6 stimulates vitronectin gene expression in vivo
D Seiffert1, M Geisterfer, J Gauldie
1Department of Pathology, McMaster University, Hamilton, Ontario, Canada.
Journal of Immunology (Baltimore, Md. : 1950)
|September 15, 1995
Summary
Vitronectin (Vn) acts as an acute phase reactant, increasing in response to inflammation. Interleukin-6 (IL-6) significantly drives the up-regulation of vitronectin gene expression during inflammatory conditions.
Area of Science:
- Biochemistry
- Immunology
- Molecular Biology
Background:
- Vitronectin (Vn) is a glycoprotein involved in cell adhesion and matrix formation.
- Its role in the acute phase response to inflammation has not been fully elucidated.
Purpose of the Study:
- To investigate whether vitronectin is regulated as an acute phase reactant.
- To determine the mechanisms underlying increased Vn synthesis during inflammation.
Main Methods:
- Measured plasma Vn levels in humans undergoing surgery.
- Induced acute inflammation in rats using LPS, CFA, and turpentine.
- Assessed hepatic Vn mRNA expression and serum Vn levels in rats.
- Administered dexamethasone and IL-6 to rats to analyze their effects on Vn mRNA.
Main Results:
- Plasma Vn concentrations doubled after surgery in humans.
- Serum Vn levels and hepatic Vn mRNA expression significantly increased in rat models of inflammation.
- Vn mRNA expression was primarily localized to hepatocytes.
- IL-6, but not dexamethasone, induced a rapid and sustained increase in hepatic Vn mRNA.
Conclusions:
- Vitronectin is up-regulated as an acute phase reactant during inflammation.
- Interleukin-6 is a primary mediator of Vn gene induction in response to inflammatory stimuli.