Hemoglobin α, NO, & Pulmonary Hypertension
By Paul Schumacker, PhD, editor, American Journal of Respiratory Cell and Molecular Biology
Follow Dr. Schumacker on Twitter @ATSRedEditor
Targeting Pulmonary Endothelial Hemoglobin α Improves Nitric Oxide Signaling and Reverses Pulmonary Artery Endothelial Dysfunction
In their December American Journal of Respiratory Cell and Molecular Biology article, Roger A. Alvarez and colleagues hypothesize that up-regulation of hemoglobin α in pulmonary endothelial cells contributes to nitric oxide depletion, which leads to vascular dysfunction in pulmonary hypertension. The authors write that a scientific consensus exists that impaired NO signaling is a culprit in NO depletion, but the mechanism behind this connection is unclear. Using human cells and mice, the researchers believe that the mechanism involves endothelial hemoglobin α, which their experiments show “functions as an endogenous scavenger of nitric oxide.”
December Highlights
Translation Review: MicroRNA Profiling in Asthma: Potential Biomarkers and Therapeutic Targets
Loss of Vascular CD34 Results in Increased Sensitivity to Lung Injury
Alda-1 Protects Against Acrolein-Induced Acute Lung Injury and Endothelial Barrier Dysfunction
Epithelial Cells Induce a Cyclo-oxygenase-1–Dependent Endogenous Reduction in Airway Smooth Muscle Contractile Phenotype
Preferential Generation of 15-HETE-PE Induced by IL-13 Regulates Goblet Cell Differentiation in Human Airway Epithelial Cells
MicroRNA-29c Prevents Pulmonary Fibrosis by Regulating Epithelial Cell Renewal and Apoptosis
Targeting Pulmonary Endothelial Hemoglobin α Improves Nitric Oxide Signaling and Reverses Pulmonary Artery Endothelial Dysfunction
