Comparative and longitudinal analysis of axial and retinal biometry in prospective models of hyperopia

Abstract

Structured AbstractPurposeTo quantify changes in axial and retinal biometry in aging hyperopic mouse models.MethodsFundus photographs and ocular biometric measurements from Mfrprd6, Prss56glcr4, Adipor1tm1Dgen, C1qtnf5tm1.1(KOMP)Vlcg and Prss56em2(IMPC)J homozygotes and C57BL/6J control mice were ascertained longitudinally up to one year of age. Parameters including axial length (AL), central corneal thickness (CCT), anterior chamber depth (ACD), lens thickness (LT), outer nuclear layer thickness (ONLT), retinal thickness (RT), vitreous chamber depth (VCD) and posterior length (PL) were measured using Spectral Domain-Optical Coherence Tomography imaging. Mixed-model analysis of variance and factorial analysis of covariance, using body size as a covariate, followed by post-hoc analysis was performed to identify significant strain differences.ResultsStrain specific changes in axial and retinal biometry along with significant effects of age, sex and body size on AL were noted. Mfrprd6, Prss56glcr4, Adipor1tm1Dgen and Prss56em2(IMPC)J homozygotes had significantly shorter AL than controls. While a comparable decrease in PL was observed in Mfrprd6, Prss56glcr4, and Adipor1tm1Dgen homozygotes, the decrease was attributed to changes in different posterior components from each mutant. Mfrprd6 and Adipor1tm1Dgen homozygotes developed regularly sized fundus spots across the ocular globe, which differed from the large bright spots seen in aged Prss56glcr4 and Prss56em2(IMPC)J homozygotes. While ONLT of C1qtnf5tm1.1(KOMP)Vlcg mice was less than controls, AL and fundus images appeared normal.ConclusionsThis study highlights differences in contributions of ocular components to AL among hyperopic mouse models with decreased AL. Understanding the mechanisms through which these proteins function, will help to elucidate their role in controlling ocular growth.