Margaret Colden-Stanfield, Ph.D.
Associate Professor

Morehouse School of Medicine
Department of Physiology, Rm MEB 349
720 Westview Drive, SW
Atlanta , GA   30310
Phone: 404-752-1678
Fax: 404-752-1055
mstanfield@msm.edu

Education
B.A.     Biology, Hampton University, Hampton , VA , 1980
Ph.D.   Pharmacology, University of Texas Medical Branch, Galveston , TX , 1986
Postdoc. Training
1986-1988, Baylor College of Medicine , Houston , TX .
1988-1990, Armed Forces Radiobiology Research Institute, Bethesda , MD.

Affiliations
Department of Physiology
Cardiovascular Research Institute

Research Interests

The primary goal of my laboratory is to characterize how ions cross the membranes of cells and to describe the ways in which these signaling mechanisms are regulated under normal and pathophysiologic conditions. We have demonstrated that there is a time-dependent increase in the expression of an inwardly rectifying K⁺ current (IKir) in human leukemia THP-1 monocytes adherent to endotoxin-treated human endothelial cells or immobilized VCAM-1 adhesion molecule. This interaction between very late activation antigen-4 (VLA-4) integrins on the surface of monocytes with vascular cell adhesion molecule-1 (VCAM-1) produces a hyperpolarization via the increased IKir to enhance the driving force for Ca²⁺ entry and thus, Ca²⁺-dependent cytokine production. Our most recent preliminary data identify an increased expression of GIRK1, GIRK4 and IRK1 mRNA that may underlie the IKir. Our immediate directions are to confirm at the RNA and protein levels the K⁺ channel species that underlies the VLA-induced whole-cell ionic currents.

Most recently, we have shifted our emphasis to bone marrow-derived macrophages to investigate the role of IKir in the activation and differentiation of monocytes into macrophages as a first step in atherosclerotic lesion formation in apoE-deficient mice as well as kidney end-organ damage in salt-induced hypertension in Dahl-salt sensitive rats. This work may lead to a better understanding of signaling events crucial to monocyte activation, differentiation, and the inflammatory response.

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