| First Author | Kim JH | Year | 2017 |
| Journal | Biochem Biophys Res Commun | Volume | 491 |
| Issue | 2 | Pages | 271-276 |
| PubMed ID | 28739257 | Mgi Jnum | J:250687 |
| Mgi Id | MGI:6103667 | Doi | 10.1016/j.bbrc.2017.07.113 |
| Citation | Kim JH, et al. (2017) Lack of epithelial PPARgamma causes cystic adenomatoid malformations in mouse fetal lung. Biochem Biophys Res Commun 491(2):271-276 |
| abstractText | Peroxisome proliferator-activated receptor-gamma (PPARgamma) plays an important role in lipid and glucose metabolism. In this study, the function of PPARgamma on lung development was investigated. Lung-specific Pparg conditional knockout mice (Pparg(DeltaLuEpC)) were developed using Cre-Lox system. Pparg(DeltaLuEpC) mice showed abnormal lung development with enlarged airspaces and followed by increase of apoptotic cells at E14.5 to E18.5. Gene analysis revealed that expression of Pmaip1, a gene related to apoptosis, was significantly increased while expression of Retnla, a gene related to anti-apoptosis, was dramatically decreased in the fetal lung (E14.5) of Pparg(DeltaLuEpC) mice. In addition, expression of Pthlh, a gene phenotypically expressed in the congenital cystic adenomatoid malformation (CCAM), was increased at E14.5 to E18.5 in the lung of Pparg(DeltaLuEpC) mice. Cell culture studies revealed that PPARgamma could bind to promoter region of Pthlh gene as a repressor in the immortalized mouse lung epithelial cell line MLE-15. Surprisingly, phenotypic changes in MLE-15-shPparg cells, stably transfected with shPparg plasmid, were similar to the Pparg(DeltaLuEpC) mice model. In addition, MLE-15-shPparg cells were easily detached from the cultured plate when cold phosphate buffered saline was applied. Furthermore, expression of Cdh1, a gene related to cell adhesion, was significantly reduced in the MLE-15-shPparg cells. Taken together, PPARgamma may play an important role in fetal lung development via alveolar cell-to-cell adhesion system. |
