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Updated: Jan 21, 2026

An Ex Vivo Tissue Culture Model for Fibrovascular Complications in Proliferative Diabetic Retinopathy
Published on: January 25, 2019
Interleukin-11 Overexpression and M2 Macrophage Density are Associated with Angiogenic Activity in Proliferative
Ahmed M Abu El-Asrar1,2, Ajmal Ahmad1, Eef Allegaert3
1Department of Ophthalmology, College of Medicine, King Saud University , Riyadh, Saudi Arabia.
Purpose:
To investigate the expression of IL-11 and its receptor IL-11Rα and to quantify density of CD163+ M2 macrophages in proliferative diabetic retinopathy (PDR).
Methods:
Vitreous samples from 29 PDR and 19 nondiabetic patients, epiretinal fibrovascular membranes from 15 patients with PDR and Müller cells were studied by enzyme-linked immunosorbent assay, immunohistochemistry and Western blot analysis.
Results:
We showed a significant increase in expression of IL-11, soluble(s) IL-11Rα, sCD163 and VEGF in vitreous samples from PDR patients compared to nondiabetic controls. Significant positive correlations were found between levels of VEGF and levels of IL-11 and sCD163. Significant positive correlations were found between microvessel density and number of blood vessels and stromal cells expressing IL-11, IL-11Rα and CD163 in PDR epiretinal membranes. The hypoxia mimetic agent cobalt chloride induced upregulation of IL-11 and IL-11Ra in cultured Müller cells.
Conclusions:
IL-11/IL-11Rα signaling and CD163+ M2 macrophages might be involved in PDR angiogenesis.
Insights
Interleukin-11 (IL-11) and Interleukin-11 receptor alpha (IL-11Rα) signaling, along with CD163-positive M2 macrophages, are implicated in proliferative diabetic retinopathy (PDR) angiogenesis. These factors show increased expression in PDR patients, correlating with disease severity.
Area of Science:
- Ophthalmology
- Immunology
- Molecular Biology
Background:
- Proliferative diabetic retinopathy (PDR) is a leading cause of vision loss.
- Diabetic retinopathy is characterized by abnormal blood vessel growth (angiogenesis).
- The role of specific molecular signaling pathways in PDR pathogenesis requires further elucidation.
Purpose of the Study:
- To investigate the expression of Interleukin-11 (IL-11) and its receptor IL-11 receptor alpha (IL-11Rα) in PDR.
- To quantify the density of CD163-positive M2 macrophages in PDR.
- To explore the relationship between IL-11/IL-11Rα and M2 macrophages in PDR.
Main Methods:
- Vitreous samples from PDR patients and nondiabetic controls were analyzed using enzyme-linked immunosorbent assay (ELISA).
- Epiretinal membranes from PDR patients and cultured Müller cells were examined via immunohistochemistry and Western blot.
- Expression levels of IL-11, IL-11Rα, soluble CD163 (sCD163), and vascular endothelial growth factor (VEGF) were quantified.
Main Results:
- Significantly elevated levels of IL-11, soluble IL-11Rα (sIL-11Rα), sCD163, and VEGF were observed in the vitreous of PDR patients compared to controls.
- Positive correlations were found between VEGF levels and IL-11/sCD163 levels, as well as between microvessel density and cells expressing IL-11, IL-11Rα, and CD163 in epiretinal membranes.
- Hypoxia induced upregulation of IL-11 and IL-11Rα in cultured Müller cells.
Conclusions:
- The IL-11/IL-11Rα signaling pathway is likely involved in the angiogenesis characteristic of PDR.
- CD163-positive M2 macrophages may play a role in the pathogenesis of PDR.
- These findings suggest potential therapeutic targets for managing PDR.
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