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

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Affiliations

  • 1. School of Life Science and Key Laboratory of the Ministry of Education for Experimental Teratology, Shandong University, Jinan 250100, China.
      Authors
    • Zhang J 1
    • Liu Z 1
    • Zhang T 1
    • Li Z 1
    • Zhang A 1
    • Sun X 1
    • Gao J 1
    (7 authors)
  • 2. Jinan First People's Hospital, Jinan 250011, China.
      Authors
    • Lin Z 2
    (1 author)

ORCIDs linked to this article

Scientific Reports, 20 Sep 2016, 6:33856
https://doi.org/10.1038/srep33856 PMID: 27645581 PMCID: PMC5029289

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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.

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