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Aldo-keto reductases in the eye.

Huang SP, Palla S, Ruzycki P, Varma RA, Harter T, Reddy GB, Petrash JM - J Ophthalmol (2010)

Bottom Line: Aldose reductase (AKR1B1) is an NADPH-dependent aldo-keto reductase best known as the rate-limiting enzyme of the polyol pathway.Some human tissues contain AKR1B1 as well as AKR1B10, a closely related member of the aldo-keto reductase gene superfamily.These results indicate that AKR1B1 and AKR1B10 may have different functional properties in the lens and suggest that AKR1B10 does not contribute to the pathogenesis of diabetic cataract in humans.

View Article: PubMed Central - PubMed

Affiliation: Department of Ophthalmology & Visual Sciences, Washington University School of Medicine, St. Louis, MO 63110, USA.

ABSTRACT
Aldose reductase (AKR1B1) is an NADPH-dependent aldo-keto reductase best known as the rate-limiting enzyme of the polyol pathway. Accelerated glucose metabolism through this pathway has been implicated in diabetic cataract and retinopathy. Some human tissues contain AKR1B1 as well as AKR1B10, a closely related member of the aldo-keto reductase gene superfamily. This opens the possibility that AKR1B10 may also contribute to diabetic complications. The goal of the current study was to characterize the expression profiles of AKR1B1 and AKR1B10 in the human eye. Using quantitative reverse transcriptase-PCR and immunohistochemical staining, we observed expression of both AKR genes in cornea, iris, ciliary body, lens, and retina. Expression of AKR1B1 was the highest in lens and retina, whereas AKR1B10 was the highest in cornea. Lenses from transgenic mice designed for overexpression of AKR1B10 were not significantly different from nontransgenic controls, although a significant number developed a focal defect in the anterior lens epithelium following 6 months of experimentally induced diabetes. However, lenses from AKR1B10 mice remained largely transparent following longterm diabetes. These results indicate that AKR1B1 and AKR1B10 may have different functional properties in the lens and suggest that AKR1B10 does not contribute to the pathogenesis of diabetic cataract in humans.

No MeSH data available.


Related in: MedlinePlus

Expression of AKR1B1 and AKR1B10 in human eye tissues. Gene transcript levels were measured by quantitative real-time PCR as described in Section 2. Data are mean ± SD among 5 nondiabetic male donors aged 65. ± 9.2 years. Data for AKR gene transcripts levels are normalized to RT-PCR for β-actin.
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Related In: Results  -  Collection


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fig1: Expression of AKR1B1 and AKR1B10 in human eye tissues. Gene transcript levels were measured by quantitative real-time PCR as described in Section 2. Data are mean ± SD among 5 nondiabetic male donors aged 65. ± 9.2 years. Data for AKR gene transcripts levels are normalized to RT-PCR for β-actin.

Mentions: The expression profiles for AKR1B1 and AKR1B10 mRNA levels were measured in cornea, iris, ciliary body, lens, and retina. Data on the apparent abundance of gene-specific transcripts were computed relative to β-actin and are shown in Figure 1. Transcripts derived from the AKR1B1 gene are present in all tissues examined, and are the highest in lens followed by retina and cornea. In the case of AKR1B10 gene transcripts, the highest transcript levels are found in cornea, with substantially lower levels found in iris, ciliary body, lens, and retina.


Aldo-keto reductases in the eye.

Huang SP, Palla S, Ruzycki P, Varma RA, Harter T, Reddy GB, Petrash JM - J Ophthalmol (2010)

Expression of AKR1B1 and AKR1B10 in human eye tissues. Gene transcript levels were measured by quantitative real-time PCR as described in Section 2. Data are mean ± SD among 5 nondiabetic male donors aged 65. ± 9.2 years. Data for AKR gene transcripts levels are normalized to RT-PCR for β-actin.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC2902055&req=5

fig1: Expression of AKR1B1 and AKR1B10 in human eye tissues. Gene transcript levels were measured by quantitative real-time PCR as described in Section 2. Data are mean ± SD among 5 nondiabetic male donors aged 65. ± 9.2 years. Data for AKR gene transcripts levels are normalized to RT-PCR for β-actin.
Mentions: The expression profiles for AKR1B1 and AKR1B10 mRNA levels were measured in cornea, iris, ciliary body, lens, and retina. Data on the apparent abundance of gene-specific transcripts were computed relative to β-actin and are shown in Figure 1. Transcripts derived from the AKR1B1 gene are present in all tissues examined, and are the highest in lens followed by retina and cornea. In the case of AKR1B10 gene transcripts, the highest transcript levels are found in cornea, with substantially lower levels found in iris, ciliary body, lens, and retina.

Bottom Line: Aldose reductase (AKR1B1) is an NADPH-dependent aldo-keto reductase best known as the rate-limiting enzyme of the polyol pathway.Some human tissues contain AKR1B1 as well as AKR1B10, a closely related member of the aldo-keto reductase gene superfamily.These results indicate that AKR1B1 and AKR1B10 may have different functional properties in the lens and suggest that AKR1B10 does not contribute to the pathogenesis of diabetic cataract in humans.

View Article: PubMed Central - PubMed

Affiliation: Department of Ophthalmology & Visual Sciences, Washington University School of Medicine, St. Louis, MO 63110, USA.

ABSTRACT
Aldose reductase (AKR1B1) is an NADPH-dependent aldo-keto reductase best known as the rate-limiting enzyme of the polyol pathway. Accelerated glucose metabolism through this pathway has been implicated in diabetic cataract and retinopathy. Some human tissues contain AKR1B1 as well as AKR1B10, a closely related member of the aldo-keto reductase gene superfamily. This opens the possibility that AKR1B10 may also contribute to diabetic complications. The goal of the current study was to characterize the expression profiles of AKR1B1 and AKR1B10 in the human eye. Using quantitative reverse transcriptase-PCR and immunohistochemical staining, we observed expression of both AKR genes in cornea, iris, ciliary body, lens, and retina. Expression of AKR1B1 was the highest in lens and retina, whereas AKR1B10 was the highest in cornea. Lenses from transgenic mice designed for overexpression of AKR1B10 were not significantly different from nontransgenic controls, although a significant number developed a focal defect in the anterior lens epithelium following 6 months of experimentally induced diabetes. However, lenses from AKR1B10 mice remained largely transparent following longterm diabetes. These results indicate that AKR1B1 and AKR1B10 may have different functional properties in the lens and suggest that AKR1B10 does not contribute to the pathogenesis of diabetic cataract in humans.

No MeSH data available.


Related in: MedlinePlus