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Inhibition of scleral proteoglycan synthesis blocks deprivation-induced axial elongation in chicks
J A Rada1, J M Johnson, V R Achen
1Department of Anatomy and Cell Biology, School of Medicine and Health Sciences, University of North Dakota, Grand Forks, ND 58202, U.S.A. jarada@medicine.nodak.edu
Insights
Inhibition of proteoglycan synthesis using beta-xyloside significantly reduced ocular elongation in chicks with form deprivation myopia. This supports the role of proteoglycans in myopia development.
Area of Science:
- Ophthalmology
- Developmental Biology
- Biochemistry
Background:
- Form deprivation myopia is characterized by ocular elongation.
- Proteoglycans are implicated in ocular tissue development and growth.
- The specific role of proteoglycan synthesis in myopia development requires further investigation.
Purpose of the Study:
- To test the hypothesis that proteoglycan synthesis contributes to ocular elongation in form deprivation myopia.
- To investigate the effect of inhibiting proteoglycan synthesis on the development of myopia in chicks.
Main Methods:
- Chicks with monocular form deprivation were treated with p-nitrophenyl-beta-D-xylopyranoside (beta-xyloside), a proteoglycan synthesis inhibitor.
- Ocular measurements (axial length, chamber depth) were performed using A-scan ultrasound.
- Scleral proteoglycans were analyzed using Sepharose CL-2B and Western blot.
Main Results:
- Beta-xyloside treatment significantly reduced axial length, vitreous chamber depth, and the rate of axial elongation in form-deprived eyes.
- No significant changes were observed in other ocular parameters or in the contralateral non-deprived eyes.
- Xyloside treatment led to the accumulation of smaller proteoglycans, including underglycosylated aggrecan.
Conclusions:
- Inhibiting scleral proteoglycan synthesis effectively reduces form deprivation-induced ocular elongation.
- These findings support the hypothesis that proteoglycan synthesis and accumulation are key drivers of axial length increases in myopia.
Abstract:
A specific inhibitor of proteoglycan synthesis was administered to chicks undergoing the development of form deprivation myopia in order to test the hypothesis that increases in proteoglycan synthesis are responsible for normal and/or deprivation-induced ocular elongation in chicks. Chicks undergoing monocular form deprivation were treated with p-nitrophenyl-beta-D-xylopyranoside (beta-xyloside) via i.p. injection every 8 hr for 5-11 days. Ocular measurements were made at the end of the experiment using high frequency A-scan ultrasound in conjunction with a LabView (v. 5.0) analysis program. Following ultrasound measurements, sclera were isolated and proteoglycans characterized by Sepharose CL-2B and Western blot analyses. Preliminary studies indicated that i.p. administration of beta-xyloside maximally inhibited sulfate incorporation into proteoglycans 8 hr after administration. Beta-xyloside treatment resulted in a significant reduction in the axial length, vitreous chamber depth, and rate of axial elongation of form deprived eyes as compared with form deprived eyes from vehicle treated chicks (P < 0.01, P < 0.05, P < 0.05, respectively). No significant differences were detected in anterior chamber depth, lens thickness, choroid thickness or retina thickness in form deprived eyes of beta-xyloside treated chicks as compared with that of vehicle controls. No significant differences were detected in contralateral non-deprived fellow eyes between beta-xyloside treated and vehicle treated chicks for any ocular measurement. Analysis of proteoglycans indicated that the xyloside treatment resulted in the accumulation of smaller proteoglycans due, in part, to the presence of underglycosylated aggrecan within the scleral matrix. These results indicate that interruption of normal scleral proteoglycan synthesis inhibits form deprivation-induced ocular elongation, supporting the hypothesis that scleral proteoglycan synthesis and accumulation are largely responsible for increases in axial length in form deprived chick eyes.
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