Thomas Steinberg,
M.D.
Associate Professor of Medicine, and Cell Biology
and Physiology
Office: (314) 362-9218
Lab: (314) 362-9219
FAX: (314) 362-9218 or 362-9230
E-mail:steinber@id.wustl.edu
Office: 8840 Wohl Clinic, Box 8051
The main research interest of this laboratory is intercellular communication in general and two families of proteins in particular. The main but by no means only cell model is the macrophage.
The first project is the role of gap junction proteins in intercellular communication. We have found that macrophages and lymphocytes express gap junction proteins; we believe that gap junction proteins function as a means of transient intercellular communication in these cells. We are also studying the expression and regulation of gap junction proteins in osteoblastic cells and in insulin-secreting cells. We have demonstrated that different gap junction proteins form aqueous channels with different molecular permeabilities, and have provided evidence that different gap junction proteins can interact to form gap junctions with unique characteristics.
The second are is the structure and function of macrophage receptors for extracellular ATP. Mouse macrophages express both the recently cloned P2Z and P2U purinergic receptors, and we have evidence for a third receptor we are currently characterizing.
A major area of interest, which encompasses both of the above projects, is the mechanism and function of intercellular calcium waves. These are rises in cytosolic calcium that pass from cell to cell. We have identified intercellular calcium waves in a variety of cell types, and have distinguished three distinct mechanisms by which these waves are propagated: autocrine activity of secreted ATP on P2U purinergic receptors (in macrophages and other cell types), activation of voltage-gated calcium channels by gap-junction mediated ionic traffic (in insulin-secreting cells), and a second gap-junction dependent mechanism that involves calcium influx but is not voltage dependent (in osteoblastic cells).