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06:15
Evaluation of Bioenergetic Function in Cerebral Vascular Endothelial Cells
Published on: November 19, 2016
Mitochondrial coupling factor 6 as a potent endogenous vasoconstrictor.
1The Second Department of Internal Medicine, Hirosaki University School of Medicine, Hirosaki, Japan. osanait@cc.hirosaki-u.ac.jp
The Journal of Clinical Investigation
|October 3, 2001
Summary
Mitochondrial coupling factor 6, a protein, acts as a circulating hormone that constricts blood vessels. This discovery may reveal a new mechanism contributing to hypertension.
Area of Science:
- Cardiovascular Biology
- Endocrinology
- Molecular Biology
Background:
- Mitochondrial coupling factor 6 (CF6) is known to suppress prostacyclin synthesis in vascular endothelial cells.
- The role of CF6 in systemic circulation and its potential as a cell surface protein were previously unexplored.
Purpose of the Study:
- To investigate if CF6 is present on the cell surface and regulates systemic circulation.
- To determine the in vivo function of CF6 in blood pressure regulation.
Main Methods:
- Detection of CF6 on CRL-2222 vascular endothelial cells and in rat plasma.
- Measurement of CF6 gene expression and plasma concentration in spontaneously hypertensive rats (SHRs) and normotensive controls.
- Administration of recombinant CF6 peptide and anti-CF6 antibody in vivo, with and without indomethacin treatment.
Main Results:
- CF6 is present on vascular endothelial cells and circulates in rat plasma.
- CF6 levels are elevated in SHRs compared to controls.
- Recombinant CF6 increased blood pressure by suppressing prostacyclin synthesis; anti-CF6 antibody decreased blood pressure, an effect blocked by indomethacin.
Conclusions:
- Mitochondrial coupling factor 6 functions as an endogenous vasoconstrictor, acting like a circulating hormone.
- CF6 may represent a novel mechanism involved in the development of hypertension.
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