Tsushima, Robert G.Virdi, Manvir Singh2020-05-112020-05-112019-102020-05-11https://hdl.handle.net/10315/37425The SNARE protein, STX1A, is expressed in various tissues. However, the role of STX1A in the heart remains unclear. Using a cardiac-specific STX1A knockout mouse model, this thesis explores the potential role of STX1A in excitation-contraction coupling. Echocardiography showed STX1A KO mice underwent transient systolic dysfunction persisting for 3 weeks. Ejection fraction and fractional shortening decreased in STX1A KO mice which returned to control levels by the 3rd week. No changes were observed in the control groups. Hypertrophy in STX1A KO hearts was not observed. Invasive hemodynamics revealed no change in LV or aortic pressures. Rate of pressure generation and relaxation were reduced in STX1A KO hearts at 0 weeks. Echocardiography also showed significant delay between the R-wave and onset of contraction in STX1A KO mice when compared to control mice. The observations of this study are indicative of STX1As role in the maintenance of normal excitation-contraction coupling in cardiomyocytes.Author owns copyright, except where explicitly noted. Please contact the author directly with licensing requests.Cellular biologyElectronic Thesis or Dissertation2020-05-11HeartMouseExcitation-contraction couplingSNARESyntaxin 1ASyntaxin 1a heart-specific knockoutEchocardiographyHemodynamics