期刊
PLOS ONE
卷 14, 期 8, 页码 -出版社
PUBLIC LIBRARY SCIENCE
DOI: 10.1371/journal.pone.0220795
关键词
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资金
- Japan Society for the Promotion of Science
- NOVARTIS Foundation (Japan) for the Promotion of Science/Japan Heart Foundation
- National Institutes of Health [HL135657]
- Takeda Science Foundation
Transforming growth factor beta (TGF-beta) has been shown to play a critical role in pathogenesis of pulmonary arterial hypertension (PAH) although the precise role of TGF-beta signaling remains uncertain. A recent report has shown that periostin (Pn) is one of the most upregulated proteins in human PAH lung compared with healthy lungs. We established type I TGF-beta receptor knockout mice specifically with Pn expressing cell (Pn-Cre/Tgfb1(fl/fl) mice). Increases in PA pressure and pulmonary artery muscularization were induced by hypoxia of 10% oxygen for 4 weeks. Lung Pn expression was markedly induced by 4 week-hypoxia. Pn-Cre/Tgfb1(fl/fl) mice showed lower right ventricular pressure elevation, inhibition of PA medial thickening. Fluorescent co-immunostaining showed that Smad3 activation in Pn expressing cell is attenuated. These results suggest that TGF-beta signaling in Pn expressing cell may have an important role in the pathogenesis of PAH by controlling medial thickening.
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