American journal of physiology. Lung cellular and molecular physiology
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ASIC1-mediated calcium entry stimulates NFATc3 nuclear translocation via PICK1 coupling in pulmonary arterial smooth muscle cells.
Chronic hypoxia limits H2O2-induced inhibition of ASIC1-dependent store-operated calcium entry in pulmonary arterial smooth muscle.
NFAT is required for spontaneous pulmonary hypertension in superoxide dismutase 1 knockout mice.
RGS3 controls T lymphocyte migration in a model of Th2-mediated airway inflammation.
Role for PKC? in enhanced endothelin-1-induced pulmonary vasoconstrictor reactivity following intermittent hypoxia.
Regulation of soluble guanylyl cyclase-alpha1 expression in chronic hypoxia-induced pulmonary hypertension: role of NFATc3 and HuR.
Cytokine-induced arginase activity in pulmonary endothelial cells is dependent on Src family tyrosine kinase activity.
Chronic hypoxia induces Rho kinase-dependent myogenic tone in small pulmonary arteries.
Reactive oxygen species mediate RhoA/Rho kinase-induced Ca2+ sensitization in pulmonary vascular smooth muscle following chronic hypoxia.
Reduced store-operated Ca2+ entry in pulmonary endothelial cells from chronically hypoxic rats.
Impaired NO-dependent inhibition of store- and receptor-operated calcium entry in pulmonary vascular smooth muscle after chronic hypoxia.
Chronic hypoxia augments protein kinase G-mediated Ca2+ desensitization in pulmonary vascular smooth muscle through inhibition of RhoA/Rho kinase signaling.
Endothelium-derived reactive oxygen species and endothelin-1 attenuate NO-dependent pulmonary vasodilation following chronic hypoxia.
Contribution of oxygen radicals to altered NO-dependent pulmonary vasodilation in acute and chronic hypoxia.
Pulmonary PKG-1 is upregulated following chronic hypoxia.
Estradiol attenuates hypoxia-induced pulmonary endothelin-1 gene expression.
Chronic hypoxia attenuates cGMP-dependent pulmonary vasodilation.
17beta-estradiol increases nitric oxide-dependent dilation in rat pulmonary arteries and thoracic aorta.
Estradiol-induced attenuation of pulmonary hypertension is not associated with altered eNOS expression.