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神经嵴细胞中Fgfr1条件性敲除诱导小鼠额骨异位软骨形成和骨形成。

Fgfr1 conditional-knockout in neural crest cells induces heterotopic chondrogenesis and osteogenesis in mouse frontal bones.

作者信息

Kawai Mariko, Herrmann David, Fuchs Alisa, Cheng Shuofei, Ferrer-Vaquer Anna, Götz Rebekka, Driller Katrin, Neubüser Annette, Ohura Kiyoshi

机构信息

Department of Pharmacology, Osaka Dental University, 8-1 Kuzuhahanazono-cho, Hirakata, Osaka, 573-1121, Japan.

Department of Developmental Biology, Institute of Biology I, University of Freiburg, Freiburg, Germany.

出版信息

Med Mol Morphol. 2019 Sep;52(3):156-163. doi: 10.1007/s00795-018-0213-z. Epub 2018 Nov 29.

Abstract

Most facial bones, including frontal bones, are derived from neural crest cells through intramembranous ossification. Fibroblast growth factor receptor 1 (Fgfr1) plays a pivotal role in craniofacial bone development, and loss of Fgfr1 leads to cleft palate and facial cleft defects in newborn mice. However, the potential role of the Fgfr1 gene in neural crest cell-mediated craniofacial development remains unclear. To investigate the role of Fgfr1 in neural crest cells, we analyzed Wnt1-Cre;Fgfr1 mice. Our results show that specific knockout of Fgfr1 in neural crest cells induced heterotopic chondrogenesis and osteogenesis at the interface of the anterior portions of frontal bones. We observed that heterotopic bone formation continued through postnatal day 28, whereas heterotopic chondrogenesis lasted only through the embryonic period. In summary, our results indicate that loss of Fgfr1 in neural crest cells leads to heterotopic chondrogenesis and osteogenesis.

摘要

大多数面骨,包括额骨,都是通过膜内成骨由神经嵴细胞发育而来。成纤维细胞生长因子受体1(Fgfr1)在颅面骨发育中起关键作用,Fgfr1缺失会导致新生小鼠出现腭裂和面部裂隙缺陷。然而,Fgfr1基因在神经嵴细胞介导的颅面发育中的潜在作用仍不清楚。为了研究Fgfr1在神经嵴细胞中的作用,我们分析了Wnt1-Cre;Fgfr1小鼠。我们的结果表明,神经嵴细胞中Fgfr1的特异性敲除在前额骨前部界面诱导了异位软骨生成和骨生成。我们观察到,异位骨形成持续到出生后第28天,而异位软骨生成仅持续到胚胎期。总之,我们的结果表明神经嵴细胞中Fgfr1的缺失会导致异位软骨生成和骨生成。

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