Inducible Endothelial <i>Gch1</i> Deletion Reveals Rapid, Sex-Specific Effects on Blood Pressure and Pregnancy Outcomes.

ABSTRACT:

Background

Tetrahydrobiopterin (BH4) is an essential cofactor for endothelial nitric oxide synthase. Constitutive endothelial BH4 deficiency leads to mild hypertension and vascular dysfunction that are partly compensated by alternative endothelium-derived vasodilators. Accordingly, we generated a novel VE-Cadherin-CreERT2 (VE-Cad-Cre) mouse to evaluate the impact of inducing endothelial-specific BH4 deficiency in adult animals, without the potential mitigating effects of developmental or other adaptive mechanisms.

Methods

Endothelial Gch1 deletion and BH4 deficiency were induced by tamoxifen administration to Gch1^fl/flVE-Cad-Cre male and female adult mice. In female mice, endothelial BH4 deficiency was also induced immediately before pregnancy

SUBMITTER: Chuaiphichai S 

PROVIDER: S-EPMC12822761 | biostudies-literature | 2026 Feb

REPOSITORIES: biostudies-literature