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Journal of Undergraduate Research

Keywords

OctN1, tobacco, COPD, cigarette smoke, lung inflammation

College

Life Sciences

Department

Physiology and Developmental Biology

Abstract

Funding available through this MEG award has provided an opportunity for me to meet many academic objectives I’ve determined to be important in the early stages of my faculty appointment at BYU. First of all, I have been able to move my on site research program forward and involve many undergraduates in the process. Specific to the current MEG award, involved students and I have been able to accomplish the proposed research. We have been successful in conducting pilot studies that reveal possible roles for OctN1 in mechanisms of lung inflammation induced by and cigarette smoke (CS). Despite improvement in personal air quality during the past few decades, the rationale for studying mechanisms leading to adverse health effects remains important. This MEG award specifically provided opportunities for students to conduct meaningful research that led to the observation that alveolar epithelial cells and bronchiolar epithelial cells increased OctN1 transcription after exposure. Because previous data reveals that molecules with binding affinity for OctN1 are also induced, it was therefore an intriguing paradigm to consider the fact that the required molecules for signaling, while basally expressed under normal conditions, can be intensely activated in both the proximal and distal lung with the appropriate trigger.

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