Endothelin-1 contributes to increased NFATc3 activation by chronic hypoxia in pulmonary arteries
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چکیده
منابع مشابه
Endothelin-1 contributes to increased NFATc3 activation by chronic hypoxia in pulmonary arteries.
Chronic hypoxia (CH) activates the Ca(2+)-dependent transcription factor nuclear factor of activated T cells isoform c3 (NFATc3) in mouse pulmonary arteries. However, the mechanism of this response has not been explored. Since we have demonstrated that NFATc3 is required for CH-induced pulmonary arterial remodeling, establishing how CH activates NFATc3 is physiologically significant. The goal o...
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RATIONALE Circulating levels of endothelin (ET)-1 and endogenous ET(A)-mediated constriction are increased in human aging. The mechanisms responsible are not known. OBJECTIVE Investigate the storage, release, and activity of ET-1 system in arteries from young and aged Fischer-344 rats. METHODS AND RESULTS After NO synthase inhibition (L-NAME), thrombin contracted aged arteries, which was in...
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Numerous cellular responses to hypoxia are mediated by the transcription factor hypoxia-inducible factor-1 (HIF-1). HIF-1 plays a central role in the pathogenesis of hypoxic pulmonary hypertension. Under certain conditions, HIF-1 may utilize feedforward mechanisms to amplify its activity. Since hypoxia increases endothelin-1 (ET-1) levels in the lung, we hypothesized that during moderate, prolo...
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Endothelin-1 (ET-1) increases pulmonary vascular tone through direct effects on pulmonary artery smooth muscle cells (PASMC) via membrane-bound ET-1 receptors. Circulating ET-1 contributes to vascular remodeling by promoting SMC proliferation and migration and inhibiting SMC apoptosis. Although endothelial cells (EC) are the primary source of ET-1, whether ET-1 produced by SMC modulates pulmona...
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ژورنال
عنوان ژورنال: American Journal of Physiology-Cell Physiology
سال: 2011
ISSN: 0363-6143,1522-1563
DOI: 10.1152/ajpcell.00029.2011