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Tomoya Morii, Takayoshi Sumioka, Masayasu Miyajima, naoki mochizuki, Shizuya Saika; The loss of S1P transporter spinster homolog 2 (Spns2) impairs morphogenesis of eyelids and meibomian glands in mice.. Invest. Ophthalmol. Vis. Sci. 2017;58(8):1743.
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To examine if the loss of spinster homolog 2 (Spns2), a cell-membrane-transporter for sphingosine 1-phosphate (S1P), affects morphogenesis of eyelids and meibomian glands. The loss of Spns2 reportedly decreases the tissue level of S1P.
Wild-type (WT) mice of C57BL/6 and Spns2-null (KO) mice (n = 4) were killed by using overdose pentobarbital, i.p. Eye and eye-adnexa including eyelids were excised and were processed for routine paraffine embedding. KO mice used were the ages of week 7, 9, 10 and 21. Deparaffinized sections were stained with hematoxylin and eosin (HE) or PAS staining, as well as immunostained for ELOVL4, PPAG-gamma, desmin or myeloperoxidase (MPO), a neutrophil marker.
Seven of 8 eyes of 4 KO mice showed an impairment of eyelid development associated with corneal scarring or opacification. HE staining histology showed severely impaired morphogenesis of meibomian glnads in KO tissue, that was further confirmed by immunostaining for ELOVL4 or PPAG-gamma, as compared with WT tissues. Orbicularis oculi muscle development was also purturbed as shown by desmin immunolocalization. No abnormal infiltration of neutrophiles was observed in KO tissue.
The loss of Spns2 impairs morphogenesis of eyelids and meibomian glands in mice. S1P signal in considered to be involved in eyelid morphogenesis.
This is an abstract that was submitted for the 2017 ARVO Annual Meeting, held in Baltimore, MD, May 7-11, 2017.
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