Theresa M. Curtis,
|Office:||1318 Bowers Hall|
|Lab:||1319 Bowers Hall|
SUNY Plattsburgh, B.S.
Albany Medical College, Ph.D.
- Anatomy and Physiology I
- Anatomy and Physiology II
- Mammalian Physiology
My lab is currently focused on two different areas of research. The first area that we are exploring is the mechanisms of mammalian wound healing after injury. Understanding how the body repairs damaged tissues, and what genes and biochemical factors influence the wound healing process will have tremendous impact on the treatment of chronic wounds and in the regeneration of healthy tissue after injury. In collaboration with Dr. Sarah Wilcox-Adelman at the Boston Biomedical Research Institute, we are investigating the mechanism of delayed wound healing in mice lacking the syndecan-4 gene. The syndecans are a family of transmembrane heparan sulfate proteoglycans that act as co-receptors with integrins and growth factor tyrosine kinase receptors. We are using cells isolated from these mice to better understand what role syndecan-4 plays in wound healing.
In addition to understanding the basic mechanisms of wound healing, my lab is also interested in natural compounds that can increase the rate of wound healing. Treatment of chronic wounds is a major public health issue that is growing because of an increase in life span, obesity, and diabetes. We have developed an in vitro model of dermal and epidermal wound healing, and have begun screening natural chemical compounds.
The second area of research in my lab is the development of the Environmental Sentinel Biomonitor (ESB) system in collaboration with the U.S. Army Center for Environmental Health Research. The goal of the ESB system is to detect a broad range of agricultural and industrial chemicals in drinking water. To accomplish this goal, a variety of cells (isolated from different tissues and organisms) are being screened for chemical toxicant sensitivity and for the ability to serve in a portable robust sensor. My lab is currently testing a variety of neuronal cell lines for inclusion in the ESB system.
Curtis, T.M., Widder, M.W., Brennan, L.M., Schwager, S.J., van der Schalie, W.H., Fey, J., Salazar, N. 2009. A portable cell based impedance sensor for toxicity monitoring in drinking water. Lab Chip, 9, 2176-2183.
Curtis, T.M., Tabb, J., Romeo, L., Schwager, S.J., Widder, M.W., van der Schalie, W.H. 2009. Improved cell sensitivity and longevity in a rapid impedance-based toxicity sensor. Journal of Applied Toxicology, vol 29(5), 374-380.
Curtis, T.M., Naal, R.M., Batt, C., Tabb, J., Holowka, D. 2008. Development of a mast cell-based biosensor. Biosensors and Bioelectronics. 23(7): 1024-1031.
Rotundo, R.F., Curtis, T.M., Shah, M.D., Gao, B., Mastrangelo, A., LaFlamme, S.E., Saba, T.M. 2002. TNF-alpha disruption of lung endothelial integrity: reduced integrin mediated adhesion to fibronectin. American Journal of Physiology. 282(2): L316-L329.
Gao, B., Curtis, T.M., Blumenstock, F.A., Minnear, F.L., Saba, T.M. 2000. Increased recycling of alpha-5 beta-1 integrins by lung endothelial cells in response to tumor necrosis factor. Journal of Cell Science. 113, 247-257.
Curtis, T.M., Rotundo, R.F., Vincent, P.A., McKeown-Longo, P.J., Saba, T.M. 1998. TNF-alpha induced matrix Fn disruption and decreased endothelial integrity are independent of Fn proteolysis. American Journal of Physiology. 275:L126-L138.
Curtis, T.M., McKeown-Longo, P.J., Vincent, P.A., Homan, S.M., Wheatley, E.M., Saba, T.M. 1995. Fibronectin attenuates the increased endothelial monolayer permeability after exposure to RGD peptides, anti-alpha-5 beta-1, or TNF-alpha. American Journal of Physiology. 269: L248-L260.