My research uses a basic understanding of molecular biology to enhance the management of patients with heart disease, and particularly those with cardiomyopathy. As a member of the Cardiomyopathy and Pulmonary Hypertension team, I am actively engaged in both clinical studies as well as basic science investigation in my lab. Bench science efforts have included using cellular and molecular biology techniques to investigate proteins, which intimately influence cardiac muscle function and excitability. Recombinant adenoviral constructs are used to express specific genes in cardiac myocytes which are then studied for changes in contractile properties. Importantly, changes in the presence of these specific proteins occur in the setting of hypertension and may influence cardiac function and progression to heart failure symptoms. My efforts in translational science focuses on the growing importance of subtle variations in the genetic code (single nucleotide polymorphisms, or SNP) having significant influence on susceptibility to disease, disease progression, and response to medical therapy.
Wilson PD, Devuyst O, Li X, Gatti L, Falkenstein D, Robinson S, Fambrough D,Burrow CR. Apical Plasma Membrane Mispolarization of NaK-ATPase in Polycystic Kidney Disease Epithelia Is Associated with Aberrant Expression of the beta2 Isoform. Am J Pathol., Jan;156(1):253-268, 2000.
Khatta M, Alexander BS, Krichten CM, Fisher ML, Freudenberger R, Robinson SW, Gottlieb SS The effect of coenzyme Q10 in patients with congestive heart failure. Ann Intern Med. Apr 18;132(8):636-40, 2000.
Freudenberger R, Sikora JA, Gottlieb S, Robinson S, Fisher M. Characteristics of patients referred for cardiac transplantation: implications for the donor organ shortage. Am Heart J. Dec;140(6):857-61, 2000.
Skotzko CE, Krichten C, Zietowski G, Alves L, Freudenberger R, Robinson S, Fisher M, Gottlieb SS. Depression is common and precludes accurate assessment of functional status in elderly patients with congestive heart failure. J Card Fail. Dec;6(4):300-5, 2000.
ICa(TTX) Channels are distinct from those generating the classical cardiac Na+ current. Chen-Izu Ye, Shorofsky SR, Robinson SW, Wier WG, Goldman L, Balke W. Biophys J. 2001 Nov;81(5):2647-59.
Blaustein MP, Golovina VA, Song H, Choate J, Lencesova L, Robinson SW, Wier WG., Organization of Ca2+ stores in vascular smooth muscle: functional implications. Novartis Found Symp 2002;246:125-37; discussion 137-41, 221-7
Sha Q, Robinson SW, McCulle SL, Shorofsky SR, Welling PA, Goldman L, Balke CW. An antisense oligonucleotide against H1 inhibits the classical sodium current but not ICa(TTX) in rat ventricular cells. J Physiol. 2003 Mar 1;547(Pt 2):435-40
Zhou X, Yin W, Doi SQ, Robinson SW, Takeyasu K, Fan X. Stimulation of Na,K-ATPase by low potassium requires reactive oxygen species. Am J Physiol Cell Physiol. 2003 Aug;285(2):C319-26.
Blaustein MP, Robinson SW, Gottlieb SS, Balke CW, Hamlyn JM. Sex, digitalis, and the sodium pump. Mol Interv. 2003 Mar;3(2):68-72.
Gottlieb SS, Khatta M, Friedmann E, Einbinder L, Katzen S, Baker B, Marshall J, Minshall S, Robinson S, Fisher ML, Potenza M, Sigler B, Baldwin C, Thomas SA. The influence of age, gender, and race on the prevalence of depression in heart failure patients. J Am Coll Cardiol. 2004 May 5;43(9):1542-9.
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