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Article Abstract
Introduction: QSOX1, a sulfhydryl oxidase involved in arterial remodelling, has recently emerged as a biomarker for preeclampsia and acute heart failure. This study sought the cardiovascular roles of Qsox1 in response to angiotensin II-induced hypertension.
Methods: With approval from an Animal Ethics Committee (CNREEA#9), two models were developed: Qsox1-invalidated adult male mice (Qsox1-/-) mice (C57BL/6J background) and a tamoxifen-inducible, vascular smooth muscle cells (VSMC)-specific Qsox1 knockout. Hypertension was induced via angiotensin II minipumps and Trans-Aortic Constriction (TAC), with assessments of cardiac function, vessel size, and VSMC phenotype.
Results: Qsox1-/- at baseline had lower blood pressure and exhibited a synthetic/immature VSMC phenotype in coronary arteries when compared to wild-type (WT). After 4 weeks of AngII infusion, Qsox1-/- mice showed acute heart failure, absent coronary media hypertrophy, and increased perivascular fibrosis compared to hypertensive WT controls (p<0.01). VSMC-specific Qsox1 knockout leading to the lack of Qsox1 in VSMC only impairing the phenotype of these cells without effecting cardiac function in response to AngII.
Conclusion: These data implicate vascular Qsox1 in the adaptive mechanisms of VSMC to pressure overload such as the development of media hypertrophy.
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