Knockout of density-enhanced phosphatase-1 impairs cerebrovascular reserve capacity in an arteriogenesis model in mice.

Knockout of density-enhanced phosphatase-1 impairs cerebrovascular reserve capacity in an arteriogenesis model in mice. Biomed Res Int. 2013;2013:802149 Authors: Hackbusch D, Dülsner A, Gatzke N, Krüger J, Hillmeister P, Nagorka S, Blaschke F, Ritter Z, Thöne-Reineke C, Böhmer FD, Buschmann I, Kappert K Abstract Collateral growth, arteriogenesis, represents a proliferative mechanism involving endothelial cells, smooth muscle cells, and monocytes/macrophages. Here we investigated the role of Density-Enhanced Phosphatase-1 (DEP-1) in arteriogenesis in vivo, a protein-tyrosine-phosphatase that has controversially been discussed with regard to vascular cell biology. Wild-type C57BL/6 mice subjected to permanent left common carotid artery occlusion (CCAO) developed a significant diameter increase in distinct arteries of the circle of Willis, especially in the anterior cerebral artery. Analyzing the impact of loss of DEP-1 function, induction of collateralization was quantified after CCAO and hindlimb femoral artery ligation comparing wild-type and DEP-1(-/-) mice. Both cerebral collateralization assessed by latex perfusion and peripheral vessel growth in the femoral artery determined by microsphere perfusion and micro-CT analysis were not altered in DEP-1(-/-) compared to wild-type mice. Cerebrovascular reserve capacity, however, was significantly impaired in DEP-1(-/-) mice. Cerebrovascular transcriptional analysis of proarteriogenic growth fa...
Source: Biomed Res - Category: Research Authors: Tags: Biomed Res Int Source Type: research