Role of Epithelial Sodium Channels and Their Regulators in Hypertension

Current position: Professor of medicine and cellular and molecular pharmacology at the University of California, San Francisco, and chief of nephrology at San Francisco General Hospital

Education: M.D. from the University of Chicago Pritzker School of Medicine in 1983; board certified in internal medicine; board eligible in nephrology

Pearce received his undergraduate degree in mathematics from the University of California, Berkeley, and received his medical degree from the University of Chicago Pritzker School of Medicine. After his residency in internal medicine at Harbor-UCLA Medical Center, he did his renal fellowship at the University of California, San Francisco.

Pearce's longstanding interest in aldosterone and mineralocorticoid receptor action began during his fellowship. With Dr. Keith Yamamoto, he demonstrated a novel mechanism for steroid receptor specificity, identifying for the first time protein-protein interactions as the principal determinant of mineralocorticoid receptor transcriptional specificity. His work on the mechanisms underlying aldosterone actions in epithelia were begun with a search for aldosterone-induced regulators of the epithelial sodium channel (ENaC). His group identified SGK1 as a serine-threonine kinase, which stimulates ENaC localization to the apical cell surface. SGK1 has become a prototype for steroid hormone action through modulation of kinase signaling cascades. Pearce's group went on to identify GILZ (glucocorticoid-induced leucine zipper protein) as an aldosterone-induced protein that stimulates ENaC by inhibiting MAP kinase signaling and recruiting SGK1 into an ENaC regulatory complex.

Read Pearce's article on page 30363.