Author Correction: Generation and comparative analysis of an Itga8-CreER T2 mouse with preferential activity in vascular smooth muscle cells

All current smooth muscle cell (SMC) Cre mice similarly recombine floxed alleles in vascular and visceral SMCs. Here we present an Itga8-CreERT2 knock-in mouse and compare its activity with a Myh11-CreERT2 mouse. Both Cre drivers demonstrate equivalent recombination in vascular SMCs. However, Myh11-CreERT2 mice, but not Itga8-CreERT2 mice, display high activity in visceral SMC-containing tissues such as intestine, show early tamoxifen-independent activity and produce high levels of CreERT2 protein. Whereas Myh11-CreERT2-mediated knockout of serum response factor (Srf) causes a lethal intestinal phenotype precluding analysis of the vasculature, loss of Srf with Itga8-CreERT2 (SrfItga8) yields viable mice with no evidence of intestinal pathology. Male and female SrfItga8 mice exhibit vascular contractile incompetence, and angiotensin II causes elevated blood pressure in wild-type, but not SrfItga8, male mice. These findings establish the Itga8-CreERT2 mouse as an alternative to existing SMC Cre mice for unfettered phenotyping of vascular SMCs after selective gene loss. Warthi et al. generated an alpha 8 integrin-cre driver that enables gene targeting preferentially in vascular smooth muscle cells (SMCs) and show, in a proof-of-principle study, that using the Itga8-CreERT2 knock-in mouse for selective ablation of the Srf gene causes vascular defects but not a lethal visceral myopathy observed in an SMC-specific Myh11-CreERT2-driven Srf loss.