Office: Roddy 285
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B.S. in Biochemistry, University of Texas
Ph.D. in Molecular and Cellular Pathology, University of North Carolina
BIOL 100 – General Biology, Lecture and Lab
BIOL 204 – Human Biology
BIOL 254 – Human Anatomy and Physiology I, Lecture and Lab
BIOL 255 – Human Anatomy and Physiology II, Lecture and Lab
BIOL 362 – Cell and Developmental Biology, Lab
AREAS OF SPECIALIZATION:
Molecular Biology, Cell Biology, Physiology, Pathology
Vascular smooth muscle cells, unlike cardiac and skeletal muscle cells, possess a unique plasticity that allows them to alternate between a contractile, differentiated state and a synthetic, proliferative state. Phenotypic switching from one state to another is beneficial for vessel maturation and injury repair, but improper control of this process contributes to atherosclerosis, restenosis, and both systemic and pulmonary hypertension. Patients with chronic obstructive pulmonary diseases, sleep apnea, and residence at high altitude have an elevated risk of developing hypoxic pulmonary hypertension due to increased pulmonary vascular resistance. Hypoxia causes pulmonary arterial smooth muscle cells (PASMCs) to undergo profound changes in phenotype, exacerbating the progression of this disease.
In our lab, we are especially interested in how hypoxia leads to structural remodeling of the pulmonary vessel wall, which is characterized by excessive PASMC proliferation and migration. Students in our lab investigate mechanisms of hypoxia-induced changes to the pulmonary vasculature using interdisciplinary approaches at the intersection of cell and molecular biology, genetics, genomics, and organ-system physiology.
SELECTED PUBLICATIONS: (* STUDENT authors)
Norton CE, Sheak JR, Yan S, Weise-Cross L, Jernigan NL, Walker BR, and Resta TC. “Augmented pulmonary vasoconstrictor reactivity following chronic hypoxia requires Src kinase and EGFR signaling.” Am J Respir Cell Mol Biol. 2019 Jul 2. PMID: 31264901.
Weise-Cross L, Resta TC, and Jernigan NL. “Redox regulation of ion channels and receptors in pulmonary hypertension.” Antioxid Redox Signal. 2018 Dec 20. PMID: 30569735
Weise-Cross L+, Sands MA+, Sheak JR, Broughton BRS, Snow JB, Gonzalez Bosc LV, Jernigan NL, Walker BR, and Resta TC. “Actin polymerization contributes to enhanced pulmonary vasoconstrictor reactivity following chronic hypoxia.” Am J Physiol Heart Circ Physiol. 2018 May 1;314(5):H1011-H1021. PMID: 29373038. *co-first authors.
Sheak JR, Weise-Cross L, deKay RJ, Walker BR, Jernigan NL, and Resta TC. “Enhanced NO-dependent pulmonary vasodilation limits increased vasoconstrictor sensitivity in neonatal chronic hypoxia.” Am J Physiol Heart Circ Physiol. 2017 Oct 1;313(4):H828-H838. PMID: 28733445
Jernigan NL, Naik JS, Weise-Cross L, Detweiler ND, Herbert LM, Yellowhair TR, and Resta TC. “Contribution of reactive oxygen species to the pathogenesis of pulmonary arterial hypertension.” PLoS One. 2017 Jun 30;12(6):e0180455. PMID: 28666030
Weise-Cross L, Taylor JM, and Mack CP. “Inhibition of diaphanous formin signaling in vivo impairs cardiovascular development and alters smooth muscle cell phenotype.” Arterioscler Thromb Vasc Biol. 2015 Nov;35(11):2374-83. PMID: 26381868
Staus DP, Weise-Cross L, Mangum KD, Medlin MD, Mangiante LE, Taylor JM, and Mack CP. “Nuclear RhoA signaling regulates MRTF-dependent SMC-specific transcription.” Am J Physiol Heart Circ Physiol. 2014 Aug 1;307(3):H379-90. PMID: 24906914