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Online Supplements Regulated Overexpression of The A1 Adenosine Receptor in Mice Results in Adverse But Reversible Changes in Cardiac Morphology And Function Hajime Funakoshi, MD, PhD; Tung O. Chan, PhD; Julie C. Good, BS; Joseph R. Libonati@, PhD; Jarkko Piuhola, MD, PhD; Xiongwen Chen$, PhD; Scott M. MacDonnell, PhD$; Ling L. Lee, MS; David E. Herrmann, BS; Jin Zhang, PhD; Jeffrey Martini, BS; Timothy M. Palmer, PhD#; Atsushi Sanbe, PhD^; Jeffrey Robbins, PhD^; Steven R. Houser, PhD$; Walter J. Koch, PhD; Arthur M. Feldman, MD, PhD Center For Translational Medicine, Department of Medicine, Jefferson Medical College, Philadelphia, PA $Cardiovascular Research Center, Temple University School of Medicine, Philadelphia, PA @Department of Kinesiology, Temple University, Philadelphia, PA Department of Internal Medicine, University of Oulu, Finland #Division of Biochemistry and Molecular Biology, Institute of Biomedical and Life Sciences, University of Glasgow, Scotland, U.K ^Division of Molecular Cardiovascular Biology, Cincinnati Childrens Hospital, Cincinnati, OH Corresponding authors: Arthur M. Feldman, MD, PhD. or Tung O. Chan, Ph.D. Department of Medicine, Jefferson Medical College 1025 Walnut Street, Suite 822 College, Philadelphia, PA 19107 Tel: 215-955-6946 Fax: 215-955-2318 E-mail: Arthur.Feldman@Jefferson.edu or Tung.Chan@mail.jci.tju.edu Short title: Regulated A1 Adenosine Receptor Transgenic Mice Methods: Transgenic mouse generation. The human A1-AR cDNA was cloned into a cardiac-specific and inducible controlled vector (TREMHC).1 As previously described, the vector promoter is composed of a modified mouse (-myosin heavy chain minimal promoter fused with nucleotide binding sites for tetracyline transactivating factor (tTA). Transgenic mice carrying the A1-AR transgene were engineered on a FVB background (PolyGene, Switzerland). Transgene expression was initiated by crossing A1-AR transgenic mice with mice that expressed tTA in the heart (MHC-tTA)