e-mail- Marc.Basson@va.gov

Education:
B.A., Philosophy of Medicine, University of Michigan, 1977
B.S., Biomedical Science, University of Michigan, 1979
M.D., University of Michigan, 1981
M.Phil., Experimental Pathology, Yale University, 1991
Ph.D., Experimental Pathology, Yale University, 1992
M.B.A., Wayne State University, 2006

Professional and Faculty Appointments:
1992-1996, Assistant Professor, Department of Surgery, Yale University
1996-2001, Associate Professor, Department of Surgery, Yale University
2001- date, Professor, Dept. of Surgery, Wayne State University
2001- date, Associate Chief of Staff for Surgical Services, John D. Dingell VA Medical Center (Joint Appointment)
2004- date, Professor, Dept. of Anesthesiology, Wayne State University (Joint Appointment)
2006- date, Professor, Dept. of Anatomy & Cell Biology, Wayne State University (Joint Appointment)

Major Research Interests:
Intestinal epithelial wound healing, cell-matrix interactions, physical force effects, cell signaling, cancer cell adhesion and metastasis

Current Research:
Intestinal epithelial wound healing is regulated by cell-matrix interactions that generate cell signals via kinases in the focal adhesion complex, including FAK (focal adhesion kinase). Although FAK has traditionally been regarded as regulated by its phosphorylation, based upon short term studies of cell signaling after adhesion to matrix proteins, we have demonstrated that FAK is critically regulated at the mRNA level during more chronic intestinal epithelial cell motility, both in vitro and in vivo. Our current studies in this area are directed at further elucidating the pathway that regulates intestinal epithelial motility, defining the critical control elements of the FAK promoter and understanding how cell motility and growth factors regulate FAK synthesis in vitro and in vivo.

A second major area of interest is the regulation of cancer cell adhesion and metastasis. In contrast to the traditional view of cancer cell adhesion as a random stochastic process regulated only by the seed and soil match between the cancer cell’s receptors and its environment, we have demonstrated that cancer cells actively regulate their own adhesion by a novel inside-out signal pathway activated by extracellular physical forces such as pressure and shear. These may be derived from iatrogenic sources during surgical procedures or from exposure to pressure and shear during passage through the circulatory or lymphatic system. Current efforts in this project are directed at further delineating this novel pathway and demonstrating its impact in vitro and in vivo. We are also pursuing in parallel studies of the effects of pressure on macrophage phagocytosis and cytokine release, as it appears that pressure stimulates macrophages by a very different signal pathway.

A third area of interest relates to a different physical force – repetitive deformation. In vitro and in vivo studies from our laboratory suggest that repetitive deformation, engendered by peristalsis, villous motility, or interaction with luminal contents, is trophic for the gut mucosa. In states of health, when intestinal cells interact primarily with a basement membrane of collagen and laminin, these forces stimulate intestinal epithelial proliferation and differentiation via FAK, Src, MAPK, and PKC. During periods of prolonged ileus or starvation, the absence of such trophic factors may contribute to the mucosal atrophy that eventually may interferes with the reintroduction of enteral nutrition. However, when acute or chronic injury expose the cells to tissue or plasma fibronectin, this acute phase reactant seems to act as a switch, altering the cellular response to repetitive deformation from a mitogenic and differentiating response to a motogenic response, adapted to restitution and the closure of mucosal wounds. Current efforts in this area are directed to understanding how this switch works in vitro and to establishing an animal model in which to study these responses in vivo.

Active Grant Support:

NIH RO1 DK067257          2005-2010 (PI)
Regulation of FAK protein in mucosal healing

NIH RO1DK060771          2005-2010 (PI)
Effect of pressure on colon cancer cell adhesion

NIH 2 T32 GM008420-14            2005-2010 (PI)
Academic Training in Trauma and Burns

VA MERIT      2004-2008 (PI)
Effect of strain on intestinal epithelial motility

Selected recent publications:

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