Molecular weight and concentration of hyaluronan in vitreous humour from diabetic patients

Autor: Kristi Granath, Ulla B.G. Laurent, Dagny Ytterberg, Karin Lilja-Englind, Per Törnquist
Rok vydání: 2009
Předmět:
Zdroj: Acta Ophthalmologica. 68:109-112
ISSN: 1755-375X
DOI: 10.1111/j.1755-3768.1990.tb01972.x
Popis: Vitreous material was collected from 24 patients undergoing pars plana vitrectomy due to hemorrhage, proliferation or traction in the vitreous body or retinal detachment. Fifteen patients had a proliferative diabets retinopathy. The non-diabetic group consisted of four patients with vascular disease: periphlebits (2), and branch vein occlusion (2) and five patients with a non-vascular disease: retinal detachment (4) and macular pucker (1). Hyaluronan analyses of the samples, which constituted about 80% of the vitreous bodies, gave values from 3 to 2600 μg, corresponding to approximately 1–700 μg/ml in situ. Low values were recorded in patients operated on for cataract and especially in those who also had retinal detachment. Molecular weight distributions of hyaluronan were determined in 8/15 diabetics and in 5/9 non-diabetics. Due to the low hyaluronan content it was not possible to perform molecular weight determination in more than one of the patients with retinal detachment. The hyaluronan was of high molecular weight in both diabetics and non-diabetics; the weight-average molecular weight (Mw) being 1.6–6.1 times 106 and 1.0–5.3 times 106, respectively. From this investigation there is no evidence that a change in the molecular properties of hyaluronan could be the cause of proliferative diabetic retinopathy. The vitreous humour contains a comparatively high concentration of hyaluronan (HYA) (100–400 μg/g). It is of high molecular weight and does not normally seem to be degraded extracellularly in the eye (Balazs & Denlinger, 1984). Proliferative diabetic retinopathy is characterized by pathological vessel formation. Recent investigations have shown that HYA can effect angiogenesis. High-molecular weight HYA seems to inhibit blood vessel formation (Feinberg & Beebe 1983, Dvorak & al 1987, West & Kumar, 1989), while oligosaccharides produced by degradation of HYA induce an angiogenic response in the chick chorioallantoic membrane (West et al, 1985). West & Kumar (1989) have also shown in vitro that vascular endothelial cells endocytose HYA, probably mediated by a receptor. They have proposed the hypothesis that vasoproliferation in diabetic patients is brought about by a change in concentration and molecular size of HYA (West & Kumar, 1988). This led us to test the hypothesis that hyaluronan is degraded in the diabetic eye and that the degradation products could be at least partly responsible for vascularization of the vitreous body. However, we find no difference in the molecular weight of HYA in diabetic and non-diabetic patients.
Databáze: OpenAIRE
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