Arginase II activity regulates cytosolic Ca2+ level in a p32-dependent manner that contributes to Ca2+-dependent vasoconstriction in native low-density lipoprotein-stimulated vascular smooth muscle cells

Abstract

Vascular disease: Controlling arterial constriction Researchers have illuminated how a protein, arginase II (ArgII), is involved in development of vascular diseases such as atherosclerosis, or narrowing of the arteries by plaque deposits. Blood vessel diameter is regulated by layers of muscle; the balance between constriction and relaxation is critical for blood flow and vascular health. Increased ArgII is known to be a factor in arterial disease; however, the details of regulation, and how they relate to plaque deposition, remain poorly understood. Sungwoo Ryoo at Kangwon National University, Chuncheon, South Korea and co-workers investigated how ArgII levels affect arterial constriction and relaxation in mice. Decreasing ArgII restored the muscle cells’ contraction response by preventing excessive calcium accumulation in the cellular powerhouse, mitochondria. These results may aid in developing treatments for one of the leading causes of death worldwide.