| First Author | Zhang J | Year | 2016 |
| Journal | Sci Rep | Volume | 6 |
| Pages | 33856 | PubMed ID | 27645581 |
| Mgi Jnum | J:239184 | Mgi Id | MGI:5825408 |
| Doi | 10.1038/srep33856 | Citation | Zhang J, et al. (2016) Loss of Lysyl Oxidase-like 3 Attenuates Embryonic Lung Development in Mice. Sci Rep 6:33856 |
| abstractText | Lysyl oxidase-like 3 (LOXL3), a human disease gene candidate, is a member of the lysyl oxidase (LOX) family and is indispensable for mouse palatogenesis and vertebral column development. Our previous study showed that the loss of LOXL3 resulted in a severe cleft palate and spinal deformity. In this study, we investigated a possible role for LOXL3 in mouse embryonic lung development. LOXL3-deficient mice displayed reduced lung volumes and weights, diminished saccular spaces, and deformed and smaller thoracic cavities. Excess elastic fibres were detected in LOXL3-deficient lungs, which might be related to the increased LOXL4 expression. Increased transforming growth factor beta1 (TGFbeta1) expression might be involved in the up-regulation of LOXL4 in LOXL3-deficient lungs. We concluded that the loss of LOXL3 attenuates mouse embryonic lung development. |
