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2017 Cardiovascular Research Day Abstract Book

51 Circadian disruption

51 Circadian disruption and atherosclerosis in ApolipoproteinE-deficient mice Eric McGann 1 • Jeffery Chalfant, MS 1 • Deborah Howatt 2 • Julie Pendergast, PhD 1 1Biology, University of Kentucky • 2 Saha Cardiovascular Research Center, University of Kentucky Staff The circadian system is a network of molecular clocks located throughout the body. These clocks coordinate daily rhythms of behavior and physiology with environmental cycles. Shift work, which chronically disrupts circadian rhythms, increases the risk of developing cardiovascular diseases. The mechanisms by which this happens, however, are largely unknown. Our long-term goal is to determine how disruption of circadian rhythms causes cardiovascular disease. Atherosclerosis is the build-up of plaques in arteries and can lead to myocardial infarction and stroke. In this study, we sought to investigate whether circadian disruption accelerates atherosclerosis in mice. Wildtype mice do not develop atherosclerotic lesions. Therefore, we studied C57BL/6J ApolipoproteinEdeficient (ApoE-/-) mice because they spontaneously develop atherosclerotic lesions. We first characterized circadian rhythms in ApoE-/- mice. We found that circadian behavioral rhythms, including free-running periods of activity in constant darkness and constant light, phase angles of entrainment, and phase shifts to light pulses, were similar between wild-type and ApoE-/- mice. These data show that ApoE-/- mice had no deficits in their circadian behavior rhythms or light responsiveness. Next, we determined if molecular circadian rhythms in tissues were altered in ApoE-/- mice. We analyzed the expression of the circadian timekeeping protein, PERIOD2, in central and peripheral tissues using a luciferase reporter. We found that PERIOD2::LUCIFERASE rhythms in tissues were similar in wild-type and ApoE-/- mice. We next determined the effect of constant light on the development of atherosclerosis in ApoE-/- mice. After 3 months in constant light, locomotor activity was arrhythmic or the rhythm was severely disrupted. In addition, atherosclerotic lesion area was increased in ApoE-/- mice in constant light compared to those in control 12h light-12h dark condition. Together, these data demonstrate that ApoE-/- mice have normal circadian rhythms and chronic circadian disruption accelerates atherosclerosis in ApoE-/- mice. This study was funded by National Institutes of Health grant P20GM103527, the Gertude F. Ribble Trust, and the University of Kentucky. 67

52 Does Light Pollution Affect the Development of Atherosclerosis? Robert Wendroth 1 • Eric McGann 1 • Deborah Howatt 2 • Julie Pendergast, PhD 1 1Department of Biology, University of Kentucky • 2 Saha Cardiovascular Research Center, University of Kentucky Undergraduate Exposure to light at night has been steadily increasing since industrialization. Light at night comes from light bulbs, light pollution produced by cities, and more recently from the widespread use of personal electronics (smart phones, tablets, laptops) at night. Previous studies in outbred mice have shown that dim light at night (DLAN) disrupts circadian rhythms and increases body weight, but it is unknown whether DLAN affects the development of cardiovascular disease. In this project, we are testing the hypothesis that DLAN accelerates the development of atherosclerotic lesions in C57BL/6J Apolipoprotein E-deficient (ApoE-/-) mice. We single-housed male ApoE-/- mice in lighttight boxes at 7 weeks of age for 1 week in 12h light:12h dark (12L:12D) and then in DLAN (12h light: 12h dim 5 lux light) for 12 weeks. Control mice were maintained in 12L:12D for 13 weeks. Body weights did not differ between ApoE-/- mice in 12L:12D and DLAN. In 12L:12D, ApoE-/- mice had a robust rhythm of eating behavior that peaked during the night. However, after a few days in DLAN, ApoE-/- mice had a low-amplitude eating behavior rhythm. Preliminary data also suggest that ApoE-/- mice in DLAN have increased atherosclerotic lesion area compared to ApoE-/- mice in 12L:12D. These data suggest that DLAN disrupts eating behavior rhythms and may also increase atherosclerosis. 68

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