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M. Wu, S. Hammad, Y. Chen, S. Zhang, J.-X. Ma, T. Lyons; Apob Leakage in Two Diabetic Retinopathy Related Animal Models. Invest. Ophthalmol. Vis. Sci. 2010;51(13):107.
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We have previously reported that intra-retinal immunofluorescence of ApoB, a marker of low density lipoprotein, exists in human type 2 diabetic retinae, to an extent correlated with severity of diabetic retinopathy (DR), but is absent in people without diabetes. In this work, we investigate whether ApoB leakage also occurs in diabetic retinopathy (DR)-related animal models: streptozotocin (STZ)-induced diabetic rats and STZ-induced diabetic hypercholesterolemic mice (C57 Black, double knockout (DKO) for the low-density lipoprotein receptor (Ldlr-/-) and the apoB mRNA editing catalytic polypeptide 1 (Apobec1-/-)).
Eight-week-old Brown Norway (BN) rats were intravenously injected with STZ (50 mg/kg in 10 mmol/L of citrate buffer, pH 4.5). Control rats received citrate buffer injection alone. Two weeks later the rats were sacrificed and retinae were stained for ApoB. In the mouse model, wild-type (WT) and DKO mice received sham or streptozotocin injections at age 7 weeks, yielding control (WT-C, DKO-C) and diabetic (WT-D, DKO-D) groups. At sacrifice (age 40 weeks), retinal ApoB was detected by immunohistochemistry.
ApoB florescence was observed in retinae from diabetic rats, predominantly in ganglion cell layer (GCL) and nerve fiber layers (NFL), but was absent in non-diabetic rats. In the mouse model, retinal ApoB was detectable by immunohistochemistry only weakly in WT mice and more strongly in the other three groups, most strongly in the GCL and inner nucleus layer (INL) adjacent to retinal vessels.
The data suggest that rodent models of diabetes exhibit leakage of lipoproteins into retinal tissues, as has been documented in retinae from people with diabetes. Animal models may serve to investigate the hypothesize that, in addition to hyperglycemia, oxidation of extravasated lipoproteins may contribute to the development of DR.
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