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. 2005 Apr;89(4):480-3.
doi: 10.1136/bjo.2004.049940.

Angiopoietin concentrations in diabetic retinopathy

J I Patel  1 , P G Hykin, Z J Gregor, M Boulton, I A Cree
Affiliations

Angiopoietin concentrations in diabetic retinopathy

J I Patel et al. Br J Ophthalmol. 2005 Apr.

Abstract

Background/aim: Angiopoietin 1 and 2 interact with vascular endothelial growth factor (VEGF) to promote angiogenesis in animal and in vitro models. Although VEGF concentrations are elevated, there is little information regarding angiopoietin concentration in the vitreous of patients with diabetic retinopathy.

Methods: Angiopoietin concentrations were measured by luminescence immunoassay in vitreous samples from 17 patients with non-proliferative diabetic retinopathy (NPDR) and clinically significant diabetic macular oedema (CSMO), 10 patients with proliferative diabetic retinopathy (PDR), and five patients with macular hole (controls) obtained at pars plana vitrectomy.

Results: Angiopoietin 1 concentrations were low in patients with macular hole (median 17 pg/ml) while in NPDR with CSMO they were 2002 pg/ml (range 289-5820 pg/ml) and in PDR 186 pg/ml (range 26-2292 pg/ml). Angiopoietin 2 concentrations in NPDR with CSMO were a median of 4000 pg/ml (range 1341-14 329 pg/ml). For both macular hole and PDR patients angiopoietin 2 was below the limit of detection.

Conclusions: Angiopoietin 2 concentration was twice that of angiopoietin 1 in NPDR with CSMO. Angiopoietin 2 is the natural antagonist of angiopoietin 1 which is thought to act as an anti-permeability agent. The predominance of angiopoietin 2 may allow VEGF induced retinal vascular permeability in patients with CSMO. The relatively low concentration of both angiopoietin 1 and 2 in patients with proliferative diabetic retinopathy may reflect the established nature of the neovascularisation in cases proceeding to vitrectomy.

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Figures

Figure 1
Figure 1
(A) Vitreous angiopoietin 1 concentration in full thickness macular hole (FTMH) (n = 5), non-proliferative diabetic retinopathy with clinically significant macular oedema (NPDR-CSMO) (n = 17), and treated proliferative diabetic retinopathy (PDR) (n = 10). The angiopoietin 1 concentration was greater in the NPDR than in FTMH and PDR (p = <0.001). (B) Vitreous angiopoietin concentration (Ang 1 and Ang 2) in non-proliferative diabetic retinopathy with clinically significant macular oedema. Angiopoietin 1 concentration was approximately half that of angiopoietin 2.
Figure 2
Figure 2
Inverse relation between vitreous angiopoietin 1 and foveal thickness. (R = −0.44, p = 0.08 Spearman correlation test) in the NPDR-CSMO patients.
Figure 3
Figure 3
Correlation of foveal thickness with aqueous angiopoietin concentrations after pars plana vitrectomy. Reduced foveal thickness (A) corresponded with an increase in angiopoietin 1 concentration (B).
Figure 4
Figure 4
Correlation of foveal thickness with aqueous angiopoietin concentrations after pars plana vitrectomy. Increased foveal thickness (A) corresponded with increased angiopoietin 2 and reduced angiopoietin 1 concentration (B).
See this image and copyright information in PMC

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