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2017 Cardiovascular Research Day Abstract Book

67 An XX Sex Chromosome

67 An XX Sex Chromosome Complement Promotes Hypercholesterolemia and Atherosclerosis in Ldlr-/- Mice Fed Western Diet Yasir Alsiraj, MS 1 • Sean Thatcher, PhD 1 • Lei Cai, PhD 2 • Ryan Temel, PhD 2 • Patrick Tso, PhD 3 • Lisa Cassis, PhD 1 1Pharmacology and Nutritional Sciences, University of Kentucky • 2 Saha Cardiovascular Research Center, University of Kentucky • 3 Department of Pathology and Laboratory Medicine, University of Cincinnati Graduate Student Objectives: Sex hormones are primary contributors to sexual dimorphism of cardiovascular diseases, but little is known about the influence of genes on sex chromosomes as mediators of cardiovascular sex differences. In this study, we hypothesized that genes on sex chromosomes influence the development of hypercholesterolemia and atherosclerosis. Methods and Results: Transgenic male mice with deletion of Sry from the Y-chromosome expressing Sry on autosomes (8-12 weeks of age) were bred to female Ldlr-/- mice to generate female and male mice with an XX or an XY sex chromosome complement. Male (M) and female (F) mice were fed a Western diet (Teklad TD88137) for 3 months. XX mice exhibited increased body weights compared to XY mice, regardless of gonadal sex (FXX, 38 ± 1.8; FXY, 30.6 ± 1.3 g; P

68 Adipocyte deficiency of ACE2 increases systolic blood pressures of obese female C57BL/6 mice Robin Shoemaker, PhD 1 • Wen Su, MD 2 • Ming Gong, PhD 2 • Lisa Cassis, PhD 1 1Pharmacology and Nutritional Sciences, University of Kentucky • 2 Physiology, University of Kentucky Postdoc Background: We demonstrated that sexual dimorphism of obesity-hypertension was associated with differential activity of adipocyte angiotensin-converting enzyme 2 (ACE2) in male versus (vs) female mice. These data suggest that adipocyte ACE2 regulates blood pressure by influencing the balance of angiotensin II (AngII, a substrate of ACE2) vs angiotensin-(1-7) (Ang-(1-7)), which differs in male and female mice. We hypothesized that deficiency of ACE2 in adipocytes increases blood pressure of HF-fed female mice. Methods/Results: Mice with adipocyte ACE2 deficiency were developed from breeding Ace2fl/fl mice to transgenic C57BL/6 mice with heterozygous transgenic expression of Cre recombinase driven by the adiponectin promoter (Ace2Adipo). Female or male Ace2fl/fl and Ace2Adipo mice (8 weeks old) were fed a HF (60% kcal as fat) or low fat (LF; 10% kcal from fat) diet for 16 weeks, after which blood pressure was quantified by radiotelemetry. Systolic blood pressures (SBP) were not different in LF-fed female mice of either genotype (24 hr average SBP [mmHg]: Ace2fl./fl: 121+/-1; Ace2Adipo: 121+/-1; p>0.05). However, SBP was significantly increased in HF-fed female Ace2Adipo vs Ace2fl/fl mice (Ace2fl/fl: 127+/-2; Ace2Adipo: 133+/-3; p

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