Role of Acid-Sensing Ion Channels in Pulmonary Vascular Smooth Muscle Store-Opera

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DESCRIPTION (provided by applicant): Dr. Nikki Jernigan earned a PhD in Biomedical Sciences from the University of New Mexico (UNM) and trained as a postdoctoral fellow in the Dept. of Physiology at the University of Mississippi and at UNM. Dr. Jernigan has published 10 first-authored manuscripts in high-quality, peer-reviewed journals. She is a member of the UNM Vascular Physiology Group, which includes six faculty members with expertise in a wide array of technical approaches ranging from whole animal studies to molecular techniques. This group holds a NHLBI-funded Cardiovascular Training Grant, and maintains an excellent record of training both graduate students and postdoctoral fellows. Drs. Walker and Resta will serve as mentors for Dr. Nikki Jernigan's research program and career development. Drs. Kanagy, Prossnitz, and Shuttleworth will serve on Dr. Jernigan's advisory committee. All have strong research programs and considerable experience in mentoring junior faculty. Under the proposed training plan, Dr. Jernigan will build upon her background in cardiovascular physiology and develop new expertise in electrophysiology and calcium imaging. Other facets of Dr. Jernigan's training will be the refinement of her presentation, teaching, writing, and critical thinking skills. The current research proposal focuses on a unique class of ion channels, acid-sensing ion channels (ASIC), and their role in mediating pulmonary vascular smooth muscle (VSM) store-operated calcium entry (SOCE). This work is significant because it will provide new insights into the mechanism of SOCE as a foundation for the regulation of pulmonary vascular resistance, which is altered in disease states such as chronic obstructive pulmonary disease (COPD) and sleep apnea. The long-term objective is to determine the contribution of ASIC-mediated SOCE contributes to elevated pulmonary vascular resistance during chronic lung diseases. Lay Relevance: The pressure in the pulmonary circulation is relatively low compared to the rest of the body. COPD is associated with increased blood pressure in the lung which places an extra workload on the heart and leads to right heart failure. Increases in pulmonary VSM basal calcium and calcium entry contribute to this elevated pressure during COPD. The proposed project will determine the role of a unique class of ion channels, in mediating calcium entry into pulmonary VSM. (End of Abstract)