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Carcinogenic agents, such as smoking, have been linked to many cancers. Recent studies show correlation to smoking-induced metastasis and fatality associated with bladder cancer. Despite many campaigns to mitigate cigarette smoke exposure, 20 percent of adults continue to smoke, providing the leading cause of preventable death U.S. In previous pilot studies, we have observed increased expression of platelet activating factor receptor (PAF-R), a member of the phospholipase A2pathway (PLA2) in response to cigarette smoke exposure. The PLA2family of enzymes are important for inflammation, angiogenesis, and cell proliferation. These observations have led to our current study, observing the effects of cigarette smoke exposure on other members in the PLA2pathway including cyclooxygenase-2 (COX-2). We examined the bladders from mice exposed to long term cigarette smoke and compared them to room air mice. We observed increased expression of COX-2 in response to cigarette smoke exposure via immunohistochemistry. To investigate whether these changes contribute to carcinogenesis, we investigated angiogenesis via pigment epithelium-derived factor (PEDF), a potent anti-angiogenic factor. Upon exposure to cigarette smoke, bladder tissue from mice demonstrated reduced expression, suggesting increased vasculature. In addition, we investigated matrix metalloproteinases (MMPs) capable of downregulating PEDF. Our studies show significant increases in MMP-2 in response to cigarette smoke, supporting our downregulated PEDF expression. Together, our results demonstrate that dysregulation of PLA2family members following cigarette smoke exposure can contribute to angiogenesis and potential tumor formation, providing beneficial therapeutic targets for bladder cancer.


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  • Subject
    • Biology

  • Institution
    • Gainesville

  • Event location
    • Floor

  • Event date
    • 22 March 2019

  • Date submitted

    19 July 2022

  • Additional information
    • Acknowledgements:

      Shannon Kispert