Logo image
Cellular, pharmacological, and biophysical evaluation of explanted lungs from a patient with sickle cell disease and severe pulmonary arterial hypertension
Journal article   Open access   Peer reviewed

Cellular, pharmacological, and biophysical evaluation of explanted lungs from a patient with sickle cell disease and severe pulmonary arterial hypertension

Natasha M Rogers, Mingyi Yao, John Sembrat, M. Patricia George, Heather Knupp, Mark Ross, Maryam Sharifi-Sanjani, Jadranka Milosevic, Claudette St. Croix, Revathi Rajkumar, …
Pulmonary circulation, Vol.3(4), pp.936-951
12/01/2013
DOI: 10.1086/674754
PMCID: PMC4070844
PMID: 25006410
url
https://doi.org/10.1086/674754View
Published (Version of record) Open Access

Abstract

Pulmonary hypertension is recognized as a leading cause of morbidity and mortality in patients with sickle cell disease (SCD). We now report benchtop phenotyping from the explanted lungs of the first successful lung transplant in SCD. Pulmonary artery smooth muscle cells (PASMCs) cultured from the explanted lungs were analyzed for proliferate capacity, superoxide (O2*−) production, and changes in key pulmonary arterial hypertension (PAH)-associated molecules and compared with non-PAH PASMCs. Upregulation of several pathologic processes persisted in culture in SCD lung PASMCs in spite of cell passage. SCD lung PASMCs showed growth factor- and serum-independent proliferation, upregulation of matrix genes, and increased O2*− production compared with control cells. Histologic analysis of SCD-associated PAH arteries demonstrated increased and ectopically located extracellular matrix deposition and degradation of elastin fibers. Biomechanical analysis of these vessels confirmed increased arterial stiffening and loss of elasticity. Functional analysis of distal fifth-order pulmonary arteries from these lungs demonstrated increased vasoconstriction to an α1-adrenergic receptor agonist and concurrent loss of both endothelial-dependent and endothelial-independent vasodilation compared with normal pulmonary arteries. This is the first study to evaluate the molecular, cellular, functional, and mechanical changes in end-stage SCD-associated PAH.
thrombospondin 1 endothelin 1 lung transplant CD47 superoxide matrix pulmonary arterial hypertension sickle cell disease

Details

Logo image