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Sci Rep. 2016 Sep 20;6:33856. doi: 10.1038/srep33856.

Loss of Lysyl Oxidase-like 3 Attenuates Embryonic Lung Development in Mice.

Author information

1
School of Life Science and Key Laboratory of the Ministry of Education for Experimental Teratology, Shandong University, Jinan 250100, China.
2
Jinan First People's Hospital, Jinan 250011, China.

Abstract

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 β1 (TGFβ1) 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.

PMID:
27645581
PMCID:
PMC5029289
DOI:
10.1038/srep33856
[Indexed for MEDLINE]
Free PMC Article

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