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Deletion of G protein-coupled receptor 48 leads to ocular anterior segment dysgenesis (ASD) through down-regulation of Pitx2
Journal article   Open access   Peer reviewed

Deletion of G protein-coupled receptor 48 leads to ocular anterior segment dysgenesis (ASD) through down-regulation of Pitx2

Jinsheng Weng, Jian Luo, Xuhong Cheng, Chang Jin, Xiangtian Zhou, Jia Qu, LiLi Tu, Di Ai, Dali Li, Jun Wang, …
Proceedings of the National Academy of Sciences - PNAS, Vol.105(16), pp.6081-6086
04/18/2008
DOI: 10.1073/pnas.0708257105
PMCID: PMC2329706
PMID: 18424556
url
https://europepmc.org/articles/pmc2329706View
Published (Version of record) Open Access

Abstract

The development of the anterior segment of the mammalian eye is critical for normal ocular function, whereas abnormal development can cause glaucoma, a leading cause of blindness in the world. We report that orphan G protein-coupled receptor 48 (Gpr48/LGR4) plays an important role in the development of the anterior segment structure. Disruption of Gpr48 causes a wide spectrum of anterior segment dysgenesis (ASD), including microphthalmia, iris hypoplasia, irdiocorneal angle malformation, cornea dysgenesis, and cataract. Detailed analyses reveal that defective iris myogenesis and ocular extracellular matrix homeostasis are detected at early postnatal stages of eye development, whereas ganglion cell loss, inner nuclear layer thinness, and early onset of glaucoma were detected in 6-month-old Gpr48 −/− mice. To determine the molecular mechanism of ASD caused by the deletion of Gpr48 , we performed gene expression analyses and revealed dramatic down-regulation of Pitx2 in homozygous knockout mice. In vitro studies with the constitutively active Gpr48 mutant receptor demonstrate that Pitx2 is a direct target of the Gpr48-mediated cAMP-CREB signaling pathway in regulating anterior segment development, suggesting a role of Gpr48 as a potential therapeutic target of ASD.
Biological Sciences cataract eye development glaucoma Lgr4

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