Education

• Undergraduate, Case Western Reserve University, Cleveland, Ohio
• Ph.D. '84, Pharmacology, New York Medical College
• Post-doctoral Fellowship, Immunology, The Scripps Research Institute
• Associate Research Scientist, Allergy and Clinical Immunology, Yale University

Honors and Awards

• Established Investigator Award, American Heart Association, 1998-2001
• Hoechst Marion Roussel Young Scholars Award, American Society of Hypertension, 1999
• Tarnower Scholar, American Heart Association, 1993-1994
• Excellence in Teaching Award (Pharmacology); New York Medical College, 1993

Research

Hypertension is an important risk factor for the development of heart disease, stroke, and kidney disease that affects greater than 40 percent of the population in the United States. Many hypertensive patients, especially African Americans, exhibit sensitivity to salt. Mechanisms that regulate salt and water transport in the kidney are critical to understanding the development of hypertension. The Ferreri laboratory is uncovering features of a novel intratubular tumor necrosis factor-alpha (TNF) system that is part of an adaptive mechanism that regulates NaCl reabsorption and blood pressure (BP) homeostasis. The production of TNF within the kidney is increased by high salt (HS) intake and decreased by low salt (LS) intake, suggesting that it may be important in salt-dependent forms of hypertension and other conditions in which salt concentrations are altered. Genetic and molecular approaches are currently being used to determine how TNF released from renal epithelial cells elicits regulatory effects in the kidney and interacts with inflammatory cells that infiltrate the kidney in response to elevated blood pressure. Dr. Ferreri recently showed that TNF inhibits intrarenal expression of angiotensinogen (AGT) by a miRNA-dependent mechanism suggesting that the intrarenal renin-angiotensin system (RAS) and TNF systems may interact with each other. The BP attenuating effect of TNF in response to HS intake is dependent upon inhibition of phospho-NKCC2 (pNKCC2) and NKCC2A expression and the molecular mechanisms that underlie these effects are currently being investigated. Collectively, the studies will define a novel intratubular regulatory system in which TNF production by renal tubular epithelial cells, in response to increases in salt intake, regulates NKCC2 isoform expression and function and contributes to BP homeostasis.

Publications

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Teaching Responsibilities

• Immunopharmacology (Course Director), Medical Pharmacology, Graduate Pharmacology