HSF II, S-012a
Education and Training
- BA, Central High School, Philadelphia, PA
- BA, University of Pennsylvania, Philadelphia, PA
- MD, University of Pennsylvania, Philadelphia, PA
- Residency, Internal Medicine, University of Pittsburgh Presbyterian University Hospital, Pittsburgh, PA
- Fellowship, Cardiology, Medical Center Hospital and University of Vermont, Burlington, VT
After completing his fellowship in cardiology, Dr. Fisher enjoyed a productive career at Case Western Reserve University in Cleveland, Ohio, before joining the University of Maryland School of Medicine faculty in 2011.
Fisher SA. Smooth Muscle Phenotypic Diversity: Effect on Vascular Function and Drug Responses. Adv Pharmacol. 2017;78:383-415. doi: 10.1016/bs.apha.2016.07.003. Epub 2016 Oct 14.
Kenchegowda D, Natale B, Lemus MA, Natale DR, Fisher SA. (2016). Inactivation of maternal Hif-1α at mid-pregnancy causes placental defects and deficits in oxygen delivery to the fetal organs under hypoxic stress. Dev Biol. 2017 Feb 15;422(2):171-185. doi: 10.1016/j.ydbio.2016.12.013. Epub 2016 Dec 9. PMID: 27940158
Reho JJ, Kenchegowda D, Asico LD, Fisher SA. A splice variant of the myosin phosphatase regulatory subunit tunes arterial reactivity and suppresses response to salt loading.
Am J Physiol Heart Circ Physiol. 2016 Jun 1;310(11):H1715-24. doi: 10.1152/ajpheart.00869.2015. Epub 2016 Apr 15. PMID: 27084390
Reho JJ, Fisher SA. The stress of maternal separation causes misprogramming in the postnatal maturation of rat resistance arteries. Am J Physiol Heart Circ Physiol. 2015 Nov;309(9):H1468-78. doi: 10.1152/ajpheart.00567.2015. Epub 2015 Sep 14. PMID: 26371173 Free PMC Article
Wang F, Fisher SA, Zhong J, Wu Y, Yang P. Superoxide Dismutase 1 In Vivo Ameliorates Maternal Diabetes Mellitus-Induced Apoptosis and Heart Defects Through Restoration of Impaired Wnt Signaling. Circ Cardiovasc Genet. 2015 Oct;8(5):665-76. doi: 10.1161/CIRCGENETICS.115.001138. Epub 2015 Jul 31. PMID: 26232087 Free PMC Article
Dr. Fisher's laboratory applies the methods of molecular biology to the study of regulation of gene expression in the development and function of the heart and vascular smooth muscle. The experiments use a wide range of techniques with a heavy reliance on novel mouse models to answer clinically relevant questions about the heart and vasculature. In one project the ODDLuciferase “hypoxia reporter” mouse and conditional KO of HIF1a, the master regulator of hypoxic transcriptional responses, is used to investigate the role of tissue hypoxia and placental dysfunction/ O2 deficits in a critical period of heart morphogenesis. In a second project the role of splice variants of the myosin phosphatase are investigated for their role in determining vaso-reactivity in various disease models. The lab has created a novel model in which the exon24 splice variant is conditionally knocked-out, thereby sensitizing vascular smooth muscle to nitric oxide and other vasodilator signals and lowering blood pressure. Dr. Fisher recently applied for a patent and is developing approaches to test this novel strategy of vasodilator sensitization for the treatment of hypertension and other vascular disorders.
Dr. Fisher obtained his research training in the laboratory of Dr. M Periasamy at the University of Vermont 1989-93, the early days of “molecular cardiology”. Since that time he has maintained an active research laboratory funded by NIH, AHA and Dept of Defense. As a practicing cardiologist-scientist he brings unique perspective to research questions that boil down to tackling cardiovascular systems level questions at the molecular level. His research has been recognized by induction into the American Society of Clinical Investigation and numerous invited reviews and presentations.
Dr. Fisher’s research interests revolve around the regulation of gene expression in relation to (a) vascular smooth muscle adaptations to altered blood flow and (b) tissue hypoxia and heart morphogenesis. Blood flow investigations focus on the regulated expression of myosin phosphatase (MP) and related contractile proteins in various models of disease in setting the sensitivity of vascular smooth muscle to signals that regulate blood flow, such as nitric oxide, reactive oxygen species, and the sympathetic nervous system. In the area of tissue hypoxia and heart morphogenesis, his research group has identified tissue oxygen gradients in the developing heart and proposed that they are required for apoptosis-dependent remodeling and patterning of the cardiac outlet structures. In addition, they may also predispose individuals to congenital heart defects.
Dr. Fisher’s laboratory work uses various techniques and equipment, including knock-out animal models; surgical models such as arterial ligations and hypoxic stress; and molecular biology techniques such as polymerase chain reaction (PCR), real-time PCR, Western blot, immunohistochemistry (IHC), plasmid cloning, subcloning and mutagenesis, RNA-protein binding assays, arrays, and immunoprecipitation. Physiology studies are conducted using vessel contractility in wire myograph and echocardiography for cardiac structure and blood flow. Bioinformatic analyses are used to assess study results.
General Cardiology: Dr. Fisher is board certified in Cardiovascular Medicine.