Ocular Phenotype of Relaxin Gene Knockout (Rln) Mice.

: To test if relaxin deficiency affects ocular structure and function we investigated expression of relaxin () and RXFP receptors (), and compared ocular phenotypes in relaxin gene knockout ( ) and wild type ( ) mice. : and mRNA expression was detected in ocular tissues of Rln+/+ mice using RT-PCR. The eyes of 11 and 5 male mice were investigated. Corneal and retinal thickness was assessed using optical coherence tomography. Intraocular pressure was measured using a rebound tonometer. Retinal, choroidal and sclera morphology and thickness were evaluated histologically. Eyes were collected and fixed for immunofluorescence staining or used for RNA extraction to evaluate mRNA expression using real-time PCR. : mRNA was expressed only in the retina, whereas transcripts were detected in the retina, cornea and sclera/choroid. was only present in the cornea. None of these genes were expressed in the lacrimal gland, eyelid or lens. Intraocular pressure was higher and central cornea of mice was significantly thicker and had significantly larger endothelial cells and a lower endothelial cell density than mice. Immunohistochemistry demonstrated no significant difference in AQP3 and AQP5 staining in the cornea or other regions between wildtype and mice. mRNA expression of was significantly higher in than in corneas, whereas and were significantly decreased. Expression of and was significantly decreased in compared to uvea. No significant differences in these genes were detected in the retina. Retinal, choroidal and scleral thicknesses were not different and morphology appeared normal. : The findings indicate that loss of affects expression of several genes in the uvea and cornea and results in thicker corneas with altered endothelial cells. Many of the gene changes suggest alterations in extracellular matrix and fluid transport between cells.