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@article{1368564, author = {Pekarová, Michaela and Koudelka, Adolf and Kolářová, Hana and Ambrožová, Gabriela and Klinke, Anna and Černá, Anna and Kadlec, Jaroslav and Trundová, Mária and Svihalkova, Lenka Sindlerova and Kuchta, Radek and Kuchtova, Zdenka and Lojek, Antonín and Kubala, Lukáš}, doi = {http://dx.doi.org/10.1016/j.vph.2015.06.005}, keywords = {Asymmetric dimethyl arginine; Pulmonary hypertension; Human pulmonary artery endothelial cell; Human pulmonary artery smooth muscle cell; Hypoxia}, issn = {1537-1891}, journal = {Vascular Pharmacology}, title = {Asymmetric dimethyl arginine induces pulmonary vascular dysfunction via activation of signal transducer and activator of transcription 3 and stabilization of hypoxia-inducible factor 1-alpha}, url = {http://www.sciencedirect.com/science/article/pii/S1537189115001366}, year = {2015} }
TY - JOUR ID - 1368564 AU - Pekarová, Michaela - Koudelka, Adolf - Kolářová, Hana - Ambrožová, Gabriela - Klinke, Anna - Černá, Anna - Kadlec, Jaroslav - Trundová, Mária - Svihalkova, Lenka Sindlerova - Kuchta, Radek - Kuchtova, Zdenka - Lojek, Antonín - Kubala, Lukáš PY - 2015 TI - Asymmetric dimethyl arginine induces pulmonary vascular dysfunction via activation of signal transducer and activator of transcription 3 and stabilization of hypoxia-inducible factor 1-alpha JF - Vascular Pharmacology SN - 15371891 KW - Asymmetric dimethyl arginine KW - Pulmonary hypertension KW - Human pulmonary artery endothelial cell KW - Human pulmonary artery smooth muscle cell KW - Hypoxia UR - http://www.sciencedirect.com/science/article/pii/S1537189115001366 N2 - Pulmonary hypertension (PH), associated with imbalance in vasoactive mediators and massive remodeling of pulmonary vasculature, represents a serious health complication. Despite the progress in treatment, PH patients typically have poor prognoses with severely affected quality of life. Asymmetric dimethyl arginine (ADMA), endogenous inhibitor of endothelial nitric oxide synthase (eNOS), also represents one of the critical regulators of pulmonary vascular functions. The present study describes a novel mechanism of ADMA-induced dysfunction in human pulmonary endothelial and smooth muscle cells. The effect of ADMA was compared with well-established model of hypoxia-induced pulmonary vascular dysfunction. It was discovered for the first time that ADMA induced the activation of signal transducer and activator of transcription 3 (STAT3) and stabilization of hypoxia inducible factor 1α (HIF-1α) in both types of cells, associated with drastic alternations in normal cellular functions (e.g., nitric oxide production, cell proliferation/Ca2+ concentration, production of pro-inflammatory mediators, and expression of eNOS, DDAH1, and ICAM-1). Additionally, ADMA significantly enhanced the hypoxia-mediated increase in the signaling cascades. In summary, increased ADMA may lead to manifestation of PH phenotype in human endothelial and smooth muscle cells via the STAT3/HIF-1α cascade. Therefore this signaling pathway represents the potential pathway for future clinical interventions in PH. ER -
PEKAROVÁ, Michaela, Adolf KOUDELKA, Hana KOLÁŘOVÁ, Gabriela AMBROŽOVÁ, Anna KLINKE, Anna ČERNÁ, Jaroslav KADLEC, Mária TRUNDOVÁ, Lenka Sindlerova SVIHALKOVA, Radek KUCHTA, Zdenka KUCHTOVA, Antonín LOJEK a Lukáš KUBALA. Asymmetric dimethyl arginine induces pulmonary vascular dysfunction via activation of signal transducer and activator of transcription 3 and stabilization of hypoxia-inducible factor 1-alpha. \textit{Vascular Pharmacology}. 2015. ISSN~1537-1891. Dostupné z: https://dx.doi.org/10.1016/j.vph.2015.06.005.
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