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H Luan, R Kowluru, P Koppolu, R Gupta, D Pacheco, M Leitges, Y Ito, B Berkowitz; PKC ßII and the Subnormal Retinal Oxygenation Response in Galactose-fed Mice . Invest. Ophthalmol. Vis. Sci. 2002;43(13):1337.
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© ARVO (1962-2015); The Authors (2016-present)
Purpose: To test the hypothesis that elevated PKC ßII expression contributes to the development of a subnormal retinal oxygenation response to a hyperoxic challenge in the galactose-fed mouse. Methods: In urethane anesthetized C57BL/6J mice, fMRI was used to measure noninvasively the change in oxygen tension (Δ;PO2) along the entire inner retina (i.e., from superior ora serrata to inferior ora serrata) during a hyperoxic inhalation challenge. In normal mice, two hyperoxic conditions were compared: 100% oxygen (n = 6) and carbogen (95% O2 : 5% CO2, n = 8). In separate experiments, fMRI and a carbogen challenge were used to examine the retinal Δ;PO2 of normal and PKC ßII knockout (KO) mice fed either regular chow (n = 8 and 5, respectively) or a 50% galactose diet for 2 months (n = 5 and 7, respectively). Protein expression of retinal PKC ßII was assessed by Western analysis. Results: In normal mice, carbogen breathing produced an increase (P < 0.05) from each other. Retinal PKC ßII protein expression was elevated in galactose fed mice and basically absence in the KO mice. The retinal Δ;PO2 of galactose-fed C57BL/6J and PKC ßII KO mice were significantly (P < 0.05) lower than that of normal and KO mice fed normal chow. Conclusion: In the galactose-fed mouse, as in our previous studies in diabetic and galactose-fed rats, a subnormal retinal Δ;PO2 was found well before the reported appearance of retinal histopathology. Although retinal PKC ßII expression is elevated in the galactose-fed mouse, we find no evidence that this isoform contributes to the development of a subnormal Δ;PO2 in the present study.
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