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Published on: February 25, 2016
Mitochondrial arginase II constrains endothelial NOS-3 activity
Hyun Kyo Lim1, Hyun Kyoung Lim, Sungwoo Ryoo
1Department of Anesthesiology, Johns Hopkins Hospital, The Johns Hopkins Medical Institutions, 600 N. Wolfe St., Baltimore, MD 21287, USA.
American Journal of Physiology. Heart and Circulatory Physiology
|September 11, 2007
Summary
Mitochondrial arginase II regulates nitric oxide (NO) production and vascular function. Its absence in mice increased NO and improved blood vessel flexibility, highlighting its role in endothelial nitric oxide synthase-3 (NOS-3) activity.
Area of Science:
- Vascular Biology
- Biochemistry
- Cellular Biology
Background:
- Arginase enzymes modulate endothelial nitric oxide synthase-3 (NOS-3) activity by controlling L-arginine availability.
- Subcellular localization and specific roles of arginase isoforms in vascular endothelial cells are not fully understood.
Purpose of the Study:
- To test if arginase II is localized in mitochondria and reciprocally regulates vascular endothelial nitric oxide (NO) production.
- To investigate the impact of mitochondrial arginase II on vascular endothelial function and stiffness.
Main Methods:
- Western blot, immunocytochemistry (MitoTracker), and immunoelectron microscopy to determine arginase II localization.
- Assessment of arginase activity and NO production in wild-type (WT) and arginase II knockout (ArgII(-/-)) mouse aortas and endothelial cells.
- Vascular function (vasorelaxation/constriction) and stiffness (pulse wave velocity) measurements in mouse carotid arteries and aorta.
Main Results:
- Arginase II was confirmed to be predominantly localized in mitochondria.
- ArgII(-/-) mice exhibited decreased arginase activity, increased NO production, enhanced vasorelaxation to acetylcholine, and attenuated vasoconstriction to phenylephrine.
- Vascular stiffness was significantly reduced in ArgII(-/-) mice compared to WT mice.
Conclusions:
- Mitochondrial arginase II plays a key role in regulating endothelial NO production and vascular endothelial function.
- Modulation of NOS-3 activity by mitochondrial arginase II impacts vascular stiffness.
- Targeting mitochondrial arginase II may offer therapeutic potential for vascular dysfunction.
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