ARG2 (arginase type II) protein, found in mitochondria, catalyzes the hydrolysis of arginine to ornithine and urea. It is widely distributed, but most highly expressed in the prostate and kidney.
This strain carries a targeted mutation of Arg2. Homozygous mutant mice exhibit hyperargininemia but are normal with respect to several related amino acids (Cit, Orn, Pro). When treated with streptozotocin to induce diabetes, homozygotes show less stiffening of the carotid artery than wildtype diabetic mice. In a model of retinopathy of prematurity (ROP) that employs Oxygen-Induced Retinopathy (OIR), homozygous mutant mice show reduced neuro-glial injury and improved retinal function. Neuronal survival and function are significantly improved and there's an inhibition of retinal thinning, preservation of rod bipolar cells and prevention of glial activation in retinas.
While homozygous mice are viable and generally fertile, it should be noted that unpublished studies suggest that there may be diminished fertility in homozygous males. Functional inactivation of the gene was confirmed by assaying the enzyme in the kidney, but Northern blotting of mRNA reveals the presence of a band similar in both intensity and size to the normal gene product. This strain may be useful in applications related to the study of arginine homeostasis, vascular dysfunction, and neurodegeneration associated with retinopathy of prematurity.
