Effect of Estrogen Receptor Antagonism on LOX Activity and Expression in Cardiac Fibroblasts
Location
Medical Education Building, LSUHSC-NO
Presentation Date
10-10-2019 10:00 AM
End Date
10-10-2019 12:00 PM
Description
Cardiovascular disease accounts for roughly a third of all deaths globally. In the United States alone, an estimated 90 million adults had some form of cardiovascular disease as of 2017. The link between cardiovascular and pulmonary diseases and cigarette smoking or nicotine usage is well established. Specifically, nicotine inhalation in mouse and human models is associated with dysfunction of the renin angiotensin system (RAS) and elevated blood pressures. Activation of RAS leads to cardiac remodeling, including hypertrophy and fibrosis. Although not known, these effects are likely due to the activation of cardiac fibroblasts. We hypothesize that nicotine causes activation of cardiac fibroblasts via angiotensin 2 signaling. To test this hypothesis, we utilize a culture model of primary adult rodent cardiac fibroblasts. Cells will be treated with nicotine in the presence and absence of antagonists of the angiotensin receptors (type 1 and/or 2). End point measures will include expression of key extracellular matrix proteins (collagens, lysyl oxidase), proliferation of cardiac fibroblasts. In addition I will conduct collagen gel contraction and wound healing functional assays.
Recommended Citation
Johnson, John C., "Effect of Estrogen Receptor Antagonism on LOX Activity and Expression in Cardiac Fibroblasts" (2019). Medical Student Research Poster Symposium. 21.
https://digitalscholar.lsuhsc.edu/sommrd/2019/posters/21
Effect of Estrogen Receptor Antagonism on LOX Activity and Expression in Cardiac Fibroblasts
Medical Education Building, LSUHSC-NO
Cardiovascular disease accounts for roughly a third of all deaths globally. In the United States alone, an estimated 90 million adults had some form of cardiovascular disease as of 2017. The link between cardiovascular and pulmonary diseases and cigarette smoking or nicotine usage is well established. Specifically, nicotine inhalation in mouse and human models is associated with dysfunction of the renin angiotensin system (RAS) and elevated blood pressures. Activation of RAS leads to cardiac remodeling, including hypertrophy and fibrosis. Although not known, these effects are likely due to the activation of cardiac fibroblasts. We hypothesize that nicotine causes activation of cardiac fibroblasts via angiotensin 2 signaling. To test this hypothesis, we utilize a culture model of primary adult rodent cardiac fibroblasts. Cells will be treated with nicotine in the presence and absence of antagonists of the angiotensin receptors (type 1 and/or 2). End point measures will include expression of key extracellular matrix proteins (collagens, lysyl oxidase), proliferation of cardiac fibroblasts. In addition I will conduct collagen gel contraction and wound healing functional assays.
Comments
Mentor: Jason Gardner PhD (Department of Physiology)