Work Description: Transient receptor potential (TRP) ion channels appear to play a key role in maintaining lung epithelial calcium homeostasis, which can be disrupted by exposure to environmental toxins. This resulting cell stress/damage triggers differential expression of TRP ankyrin-1 (TRPA1) and TRP vanilloid-3 (TRPV3). TRPV3 expression is transiently increased while TRPA1 is suppressed. However, TRPA1 is subsequently induced as TRPV3 decreases, and this dynamic is crucial for limiting cell damage and restoration of homeostasis. The control mechanism for this is phenomenon is unknown but may be coordinated by growth factor and kinase/phosphatase signaling. My project seeks to elucidate this control mechanism with the long-term goal of identifying therapeutic opportunities to protect cells from damage and the effects of environmental pollutants on diseases such as asthma and chronic obstructive pulmonary disease (COPD).