期刊
SCIENTIFIC REPORTS
卷 6, 期 -, 页码 -出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/srep33856
关键词
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资金
- National Natural Science Foundation of China [81670943, 30871436, 30973297, 31171194]
- National Basic Research Program (973) of China [2010CB945002, 2014CB541703]
- Shandong Provincial Science and Technology Key Program [2009GG10002039]
- Shandong Provincial Natural Science Foundation of China [ZR2013CQ041]
- Independent Innovation Foundation of Shandong University Grants, IIFSDU [2013GN011]
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 beta 1 (TGF beta 1) 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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