Dr. Laura Weise Cross

EDUCATION:
B.S. in Biochemistry, University of Texas
Ph.D. in Molecular and Cellular Pathology, University of North Carolina

COURSES TAUGHT:
BIOL 100 – General Biology, Lecture and Lab
BIOL 204 – Human Biology
BIOL 207 – Human Sexuality
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

RESEARCH INTEREST(S):
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.

STUDENT RESEARCH:
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)
Snow JB, Norton CE, Sands MA, Weise-Cross L, Yan S, Herbert LM, Sheak JR, Gonzalez Bosc LV, Walker BR, Kanagy NL, Jernigan NL, Resta TC. “Intermittent hypoxia augments pulmonary vasoconstrictor reactivity through PKC/mitochondrial oxidant signaling.” Am J Respir Cell Mol Biol. 2020 Jun; 62(6):732-746. PMID: 32048876 DOI: 10.1165/rcmb.2019-0351OC

Norton CE, Weise-Cross L, Ahmadian R, Yan S, Jernigan NL, Paffett ML, Naik JS, Walker BR, Resta TC. “Altered lipid domains facilitate enhanced pulmonary vasoconstriction following chronic hypoxia.” Am J Respir Cell Mol Biol. 2020 Jun; 62(6):709-718. PMID: 31945301 DOI: 10.1165/rcmb.2018-0318OC 

Sheak JR, Yan S, Weise-Cross L, Ahmadian R, Walker BR, Jernigan NL, Resta TC. “PKC and reactive oxygen species mediate enhanced pulmonary vasoconstrictor reactivity following chronic hypoxia in neonatal rats.” Am J Physiol Heart Circ Physiol. 2020 Feb 1;318(2):H470-H483. PMID: 31922892 DOI: 10.1152/ajpheart.00629.2019

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 DOI: 10.1165/rcmb.2018-0106OC

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 DOI: 10.1089/ars.2018.7699

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 DOI: 10.1152/ajpheart.00664.2017*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 DOI: 10.1152/ajpheart.00123.2017

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 DOI: 10.1371/journal.pone.0180455

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 DOI: 10.1161/ATVBAHA.115.305879

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 DOI: 10.1152/ajpheart.01002.2013