Dr. BARBARA SAFIEJKO-MROCZKA Assistant Professor E-mail: bsafiejko@ou.edu Office Phone: (405) 325-6192 RM/Lab: RH 261/310 Webpage: http://faculty-staff.ou.edu/S/Barbara.Safiejko-Mroczk-1/

Courses:

Histology ZOO 4244

Cellular Pathology ZOO 4970/5970

Research Interests

My research focuses on cellular mechanisms of wound healing and the role of cell motility and the cytoskeleton in this process. Cell migration, proliferation, formation and disassembly of cell-substratum adhesions are essential events in wound healing. In the in vivo state, several types of cells and components of extracellular matrix (ECM) are involved in the wound healing process. Fibroblasts play a number of important roles in wound healing – they migrate into the wound, proliferate, synthesize components of ECM and contribute greatly to wound closure and tissue remodeling by exerting contractile forces on ECM fibers. Cytoskeleton plays an essential role in cell motility and contributes to the formation of adhesions. Cellular migration and rapid proliferation are dependent on the presence of chemotactic and mitogenic agents that attract cells to the wound space and stimulate cell division in the wound microenvironment.
The wound healing is highly impaired in diabetics. I am interested in studying the effects of hyperglycemic conditions (similar to those present in diabetic state) on wound healing in vitro. Cell migration, proliferation, formation and disassembly of cell-substratum adhesions and organization of the cytoskeleton are studied in physiologic and diabetic conditions using in vitro wound models (cells grown as monolayer and cells cultured in a reconstituted matrix closely resembling the wound environment in vivo). Also effects of specific growth factors and cytokines on the dynamics of wound healing are studied using these models.
One of the major complications of diabetes mellitus is increased incidence and severity of periodontitis. Oral bacteria and their products (toxins, lipopolysaccharides, gingipains) are present and have impact on the behavior of cells within the periodontium. One of the ongoing projects is focused on the effects of bacterial products on wound healing and cell motility using in vitro model.
I am also interested in improving and developing new methods of specimen preparation for fluorescence, light, and high resolution scanning and transmission electron microscopy.

Distribution of vinculin (red) and F-actin (green) in human gingival fibroblast

 

Selected publications:

• Safiejko-Mroczka, B. and P.B. Bell. 1995. The induction of protrusion by neomycin in human glioma cells is correlated with a decrease followed by an increase in filamentous actin. Cell Biology International 19: 655-674.
  
• Bell, P.B. and B. Safiejko-Mroczka. 1995. Visualization of macromolecular structures by fluorescence and scanning electron microscopy. Scanning Microscopy 9 (3):943-960.
  
• Safiejko-Mroczka, B. and P.B. Bell. 1996. Bifunctional protein crosslinking reagents improve labeling of cytoskeletal proteins for qualitative and quantitative fluorescence microscopy. Journal of Histochemistry and Cytochemistry 44(6):641-656.
  
• Bell, P.B. and B. Safiejko-Mroczka. 1997. Preparing whole mounts of biological specimens for imaging macromolecular structures by light and electron microscopy. International Journal of Imaging Systems and Technology 8:225-239.
  
• Bell, P.B. and B. Safiejko-Mroczka. 1997. Using bifunctional protein crosslinking reagents to enhance the preservation of cytoskeletal proteins for light and electron microscopy. Pierce Previevs 1 (2):8-13.
  
• Safiejko-Mroczka, B. and P.B. Bell. 1998. Distribution of cytoskeletal proteins in neomycin-induced protrusions of human fibroblasts. Experimental Cell Research 242:495-514.
  
• Safiejko-Mroczka, B. and P.B. Bell. 2001. The effects of neomycin on cell motility and the actin cytoskeleton in human fibroblasts. Cell Motility and the Cytoskeleton 50:13-32.
  
• M. Qa Dan, M. Ramsey, J. Daniel, L. Spyres, B. Safiejko-Mroczka, W. Ortiz-Leduc and J. Ballard. 2002. Clostridium difficile toxin B activates dual caspase-dependent and caspase-independent apoptosis in intoxicated cells. Cellular Microbiology 4 (7): 425-434.
   

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