Abstract 10789: Disruption of Stromal Interaction Molecule 1 in Immune Regulatory T Cells Protects Vascular Endothelial Function in Renovascular Hypertension

Abstract

Introduction & Hypothesis: Microvascular dysfunction in renovascular hypertension is a major risk factor for cardiovascular diseases. However, the underlying mechanism of vascular endothelial dysfunction in renovascular hypertension is not fully understood. Here, we sought to determine the role and impact of the stromal interaction molecule 1 (STIM1) knockout in immune regulatory T cells (Stim1 Treg-/- ) in renovascular hypertension-induced vascular endothelial dysfunction. Methods: Mice were divided into four groups. Group 1 and 2: Stim1 flx/flx male and female mice with and without 2-kidney-1-clip (2K1C) surgery for four weeks. Group 3 and 4: Stim1 Treg-/- male and female mice with and without 2K1C for four weeks. We measured body weight, arterial blood pressure, cardiac hypertrophy, lung edema, inflammation, fibrosis, and assessed microvascular endothelial function. Results: Stim1 flx/flx both male and female mice subjected to 2K1C for four weeks develop hypertension, cardiac hypertrophy, lung edema, low running performance, and vascular dysfunction. Interestingly, the disruption of STIM1 in Treg cells in both male and female mice protected from 2K1C-induced hypertension, cardiac hypertrophy, and lung edema. Moreover, microvascular endothelial function was also protected in both groups. Conclusion: Our data illustrate that STIM1 in immune Treg cells has s significant impact in renovascular hypertension-induced cardiovascular complications. Thus, targeting STIM1 in Treg cells could be a potential therapeutic approach to protect from renovascular hypertension-induced cardiovascular diseases.