| First Author | Seki M | Year | 2019 |
| Journal | PLoS One | Volume | 14 |
| Issue | 8 | Pages | e0220795 |
| PubMed ID | 31437169 | Mgi Jnum | J:278762 |
| Mgi Id | MGI:6359163 | Doi | 10.1371/journal.pone.0220795 |
| Citation | Seki M, et al. (2019) Periostin-expressing cell-specific transforming growth factor-beta inhibition in pulmonary artery prevents pulmonary arterial hypertension. PLoS One 14(8):e0220795 |
| abstractText | 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/Tgfb1fl/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/Tgfb1fl/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. |
