PDF(Pubmed)
Abstract：
The mouse Harderian gland (HG) is a secretory gland that covers the posterior portion of the eyeball, opening at the base of the nictitating membrane. The HG serves to protect the eye surface from infection with its secretions. Mice open their eyelids at about 2 weeks of age, and the development of the HG primordium mechanically opens the eye by pushing the eyeball from its rear. Therefore, when HG formation is disturbed, the eye exhibits enophthalmos (the slit-eye phenotype), and a line of Fgf10+/- heterozygous loss-of-function mice exhibits slit-eye due to the HG atrophy. However, it has not been clarified how and when HGs degenerate and atrophy in Fgf10+/- mice. In this study, we observed the HGs in embryonic (E13.5 to E19), postnatal (P0.5 to P18) and 74-week-old Fgf10+/- mice. We found that more than half of the Fgf10+/- mice had markedly degenerated HGs, often unilaterally. The degenerated HG tissue had a melanized appearance and was replaced by connective tissue, which was observed by P10. The development of HGs was delayed or disrupted in the similar proportion of Fgf10+/- embryos, as revealed via histology and the loss of HG-marker expression. In situ hybridization showed Fgf10 expression was observed in the Harderian mesenchyme in wild-type as well as in the HG-lacking heterozygote at E19. These results show that the Fgf10 haploinsufficiency causes delayed or defective HG development, often unilaterally from the unexpectedly early neonatal period.
摘要：
小鼠Harderian腺（HG）是覆盖眼球后部的分泌腺，在硝化膜的底部开口。HG用于保护眼睛表面免受其分泌物的感染。老鼠在大约2周龄时睁开眼睑，HG原基的发展通过从眼球的后部推动眼球来机械地打开眼睛。因此,当HG形成受到干扰时，眼睛表现出眼球内陷（裂眼表型），和一系列Fgf10+/-杂合功能丧失小鼠由于HG萎缩而表现出裂眼。然而,尚不清楚HGs在Fgf10/-小鼠中如何以及何时退化和萎缩。在这项研究中,我们观察了胚胎中的HG（E13.5至E19），出生后（P0.5至P18）和74周龄Fgf10+/-小鼠。我们发现，超过一半的Fgf10+/-小鼠具有明显退化的HGs，往往是单方面的。退化的HG组织有黑化的外观，被结缔组织取代，这是由P10观察到的。在相似比例的Fgf10+/-胚胎中，HGs的发育被延迟或破坏，如通过组织学和HG标记表达的丧失所揭示的。原位杂交显示，在野生型Harderian间质中以及在E19缺乏HG的杂合子中观察到Fgf10表达。这些结果表明，Fgf10单倍体不足导致HG发育延迟或缺陷，通常从意外的早期新生儿期单方面开始。
