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.

Agency
National Institute of Health (NIH)
Institute
National Heart, Lung, and Blood Institute (NHLBI)
Type
Research Scientist Development Award - Research & Training (K01)
Project #
5K01HL092598-02
Application #
7619579
Study Section
Special Emphasis Panel (ZHL1-CSR-G (F1))
Program Officer
Colombini-Hatch, Sandra
Project Start
2008-05-01
Project End
2013-04-30
Budget Start
2009-05-01
Budget End
2010-04-30
Support Year
2
Fiscal Year
2009
Total Cost
$151,069
Indirect Cost
Name
University of New Mexico
Department
Physiology
Type
Schools of Medicine
DUNS #
868853094
City
Albuquerque
State
NM
Country
United States
Zip Code
87131
Jernigan, Nikki L (2015) Smooth muscle acid-sensing ion channel 1: pathophysiological implication in hypoxic pulmonary hypertension. Exp Physiol 100:111-20
Plomaritas, Danielle R; Herbert, Lindsay M; Yellowhair, Tracylyn R et al. (2014) Chronic hypoxia limits H2O2-induced inhibition of ASIC1-dependent store-operated calcium entry in pulmonary arterial smooth muscle. Am J Physiol Lung Cell Mol Physiol 307:L419-30
Nitta, Carlos H; Osmond, David A; Herbert, Lindsay M et al. (2014) Role of ASIC1 in the development of chronic hypoxia-induced pulmonary hypertension. Am J Physiol Heart Circ Physiol 306:H41-52
Norton, Charles E; Broughton, Brad R S; Jernigan, Nikki L et al. (2013) Enhanced depolarization-induced pulmonary vasoconstriction following chronic hypoxia requires EGFR-dependent activation of NAD(P)H oxidase 2. Antioxid Redox Signal 18:1777-88
Jernigan, Nikki L; Herbert, Lindsay M; Walker, Benjimen R et al. (2012) Chronic hypoxia upregulates pulmonary arterial ASIC1: a novel mechanism of enhanced store-operated Ca2+ entry and receptor-dependent vasoconstriction. Am J Physiol Cell Physiol 302:C931-40
Norton, Charles E; Jernigan, Nikki L; Kanagy, Nancy L et al. (2011) Intermittent hypoxia augments pulmonary vascular smooth muscle reactivity to NO: regulation by reactive oxygen species. J Appl Physiol (1985) 111:980-8
Resta, Thomas C; Broughton, Brad R S; Jernigan, Nikki L (2010) Reactive oxygen species and RhoA signaling in vascular smooth muscle: role in chronic hypoxia-induced pulmonary hypertension. Adv Exp Med Biol 661:355-73
Broughton, Brad R S; Jernigan, Nikki L; Norton, Charles E et al. (2010) Chronic hypoxia augments depolarization-induced Ca2+ sensitization in pulmonary vascular smooth muscle through superoxide-dependent stimulation of RhoA. Am J Physiol Lung Cell Mol Physiol 298:L232-42
Jernigan, Nikki L; Paffett, Michael L; Walker, Benjimen R et al. (2009) ASIC1 contributes to pulmonary vascular smooth muscle store-operated Ca(2+) entry. Am J Physiol Lung Cell Mol Physiol 297:L271-85
Jernigan, Nikki L; Walker, Benjimen R; Resta, Thomas C (2008) Reactive oxygen species mediate RhoA/Rho kinase-induced Ca2+ sensitization in pulmonary vascular smooth muscle following chronic hypoxia. Am J Physiol Lung Cell Mol Physiol 295:L515-29