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Changes in human bladder epithelial cell gene expression associated with interstitial cystitis or antiproliferative
Susan Keay1, Francoise Seillier-Moiseiwitsch, Chen-Ou Zhang
1Division of Infectious Diseases, Department of Medicine, University of Maryland School of Medicine, Baltimore, MD 21201, USA. skeay@medicine.umaryland.edu
Physiological Genomics
|July 9, 2003
Summary
Interstitial cystitis (IC) involves abnormal bladder epithelial cell proliferation. Antiproliferative factor (APF) in IC cells may inhibit proliferation by altering gene expression, suggesting a less proliferative phenotype.
Area of Science:
- Urology
- Cell Biology
- Molecular Biology
Background:
- Interstitial cystitis (IC) is characterized by abnormal bladder epithelial cell proliferation.
- Differences observed include antiproliferative factor (APF) production and altered growth factor expression.
Purpose of the Study:
- To investigate the role of APF in abnormal bladder epithelial cell proliferation in IC.
- To compare gene expression patterns in IC cells versus normal cells and APF-treated normal cells.
Main Methods:
- Microarray analysis of gene expression in normal bladder epithelial cells treated with APF vs. mock APF.
- Comparison of gene expression patterns between IC and normal bladder epithelial cells.
- Immunohistochemistry to confirm differential expression of specific genes.
Main Results:
- Thirteen genes involved in proliferation/differentiation were differentially expressed in both IC and APF-treated cells.
- Gene expression patterns suggested a less proliferative phenotype in IC and APF-treated cells.
- Increased expression of E-cadherin and decreased expression of vimentin were confirmed by immunohistochemistry.
Conclusions:
- APF may inhibit cell proliferation in IC by downregulating genes that stimulate proliferation and upregulating genes that inhibit growth.
- These findings support the reduced proliferation rate observed in IC and APF-treated cells.
- The study elucidates a potential mechanism for APF's role in IC pathogenesis.