Start Date
31-3-2023 10:30 AM
End Date
31-3-2023 12:30 PM
Document Type
Poster
Abstract
Inflammatory bowel disease (IBD) is an autoimmune disease of unknown cause and includes conditions such as Crohn’s disease and ulcerative colitis. With no cure and only palliative therapies available, many patients with these conditions struggle with diarrhea, abdominal pain, and other chronic symptoms. This study is interested in investigating the multidrug resistance gene (MDR) which encodes the small molecule pump P-glycoprotein (P-gp).
This gene is responsible for regulating drug absorption and accumulation in various parts of the body such as the intestines which is of particular interest to this study. Polymorphisms of the MDR1 gene (encoding p-glycoprotein) have consequently been linked to IBD in humans. We hypothesized that MDR1 deficient Caco-2 intestinal cells would heal wounds slower than control Caco-2 cells, resulting in increased leakage between the tight junctions of the intestines and an increase in disease progression.
Surprisingly, The MDR deficient cells have shown increased wound healing compared to control cells. To determine the mechanism by which the MDR deficient cells were healing wounds faster, we investigated cellular proliferation and analyzed the cellular shapes and sizes of the MDR deficient cells relative to control cells. Using the MTT (3-[4,5-dimethylthiazol-2-yl]-2,5 diphenyl tetrazolium bromide) cell proliferation assay, we detected a difference in proliferation between the MDR deficient and control cells at various time points. We also performed membrane staining which allowed us to visualize and determine the changes in cellular shape and size between the deficient and control cells.
These experimental techniques ultimately [TS1] revealed changes in proliferation for the MDR deficient cells when compared to the control Caco-2 cells as well as differences in the cellular shapes and sizes of these deficient cells. Currently, we are investigating the integrity of the barrier formed by MDR deficient cells after the wound healing is complete.
The changes we detected suggest that the wound healing mechanism differs when MDR is missing from cells, which, in the intestine, could lead to the development of inflammatory bowel disease.
Included in
MC-02 Increased wound healing in p-glycoprotein deficient intestinal cells
Inflammatory bowel disease (IBD) is an autoimmune disease of unknown cause and includes conditions such as Crohn’s disease and ulcerative colitis. With no cure and only palliative therapies available, many patients with these conditions struggle with diarrhea, abdominal pain, and other chronic symptoms. This study is interested in investigating the multidrug resistance gene (MDR) which encodes the small molecule pump P-glycoprotein (P-gp).
This gene is responsible for regulating drug absorption and accumulation in various parts of the body such as the intestines which is of particular interest to this study. Polymorphisms of the MDR1 gene (encoding p-glycoprotein) have consequently been linked to IBD in humans. We hypothesized that MDR1 deficient Caco-2 intestinal cells would heal wounds slower than control Caco-2 cells, resulting in increased leakage between the tight junctions of the intestines and an increase in disease progression.
Surprisingly, The MDR deficient cells have shown increased wound healing compared to control cells. To determine the mechanism by which the MDR deficient cells were healing wounds faster, we investigated cellular proliferation and analyzed the cellular shapes and sizes of the MDR deficient cells relative to control cells. Using the MTT (3-[4,5-dimethylthiazol-2-yl]-2,5 diphenyl tetrazolium bromide) cell proliferation assay, we detected a difference in proliferation between the MDR deficient and control cells at various time points. We also performed membrane staining which allowed us to visualize and determine the changes in cellular shape and size between the deficient and control cells.
These experimental techniques ultimately [TS1] revealed changes in proliferation for the MDR deficient cells when compared to the control Caco-2 cells as well as differences in the cellular shapes and sizes of these deficient cells. Currently, we are investigating the integrity of the barrier formed by MDR deficient cells after the wound healing is complete.
The changes we detected suggest that the wound healing mechanism differs when MDR is missing from cells, which, in the intestine, could lead to the development of inflammatory bowel disease.