Generation and Comparative Analysis of an Itga8-CreER T2 Mouse with Preferential Activity in Vascular Smooth Muscle Cells

All current smooth muscle cell (SMC) mice similarly recombine floxed alleles in vascular and visceral SMCs. Here, we present an knock-in mouse and compare its activity with a mouse. Both drivers demonstrate equivalent recombination in vascular SMCs. However, mice, but not mice, display high activity in visceral SMC-containing tissues such as intestine, show early tamoxifen-independent activity, and produce high levels of CreER protein. Whereas -mediated knockout of serum response factor ( ) causes a lethal intestinal phenotype precluding analysis of the vasculature, loss of with ( ) yields viable mice with no evidence of intestinal pathology. Male and female mice exhibit vascular contractile incompetence, and angiotensin II causes elevated blood pressure in wild type, but not , male mice. These findings establish the mouse as an alternative to existing SMC mice for unfettered phenotyping of vascular SMCs following selective gene loss.