Related Experiment Video
Updated: Jun 25, 2026

Characterization of a Novel Human Organotypic Retinal Culture Technique
Published on: June 9, 2021
Proliferative diabetic retinopathy-The influence of diabetes control on the activation of the intraocular molecule
Joanna Adamiec-Mroczek1, Jolanta Oficjalska-Młyńczak, Marta Misiuk-Hojło
1Department of Ophthalmology, Wroclaw Medical University, ul. Chałubińskiego 2a, 50-368 Wrocław, Poland. j.adamiec@wp.pl
Aims:
Demonstrate the influence of type 2 diabetes control on the degree of retinal endothelial damage (vWF, E-selectin) and local increases in the concentrations of selected adhesion molecules (ICAM-1, VCAM-1, E-selectin) in proliferative diabetic retinopathy (PDR).
Methods:
Vitreous and serum samples were collected during vitrectomy from 19 patients with PDR and 15 patients who underwent vitrectomy for other reasons. Tests were performed using the ELISA method.
Results:
Serum and intraocular concentrations of ICAM-1, VCAM-1, E-selectin, vWF were considerably higher in the subjects with PDR than in the controls. In the vitreous, the increase in vWF depended on the elevated levels of vWF in the serum (r=0.905, p<0.001). E-selectin correlated with diastolic blood pressure (r=0.506, p=0.045). The concentrations of vWF and E-selectin in both samples were related to the significant increases in intraocular ICAM-1, ICAM-1, VCAM-1 in the serum of PDR patients. Increased VCAM-1 level in the vitreous correlated with the concentration of HbA(1)c (r=0.59, p=0.007).
Conclusions:
Upon local and systemic damage to the endothelium there were significant increases in ICAM-1, VCAM-1, E-selectin. A significant positive correlation of VCAM-1 increase in the vitreous with HbA(1)c is an important argument for the influence of diabetes on immuno-inflammatory activation in the retinal microcirculation.
Related Concept Videos
Diabetic Retinopathy
Type I Diabetes II: Pathophysiology
Diabetic Nephropathy
Type II Diabetes II: Pathophysiology
Pathophysiology of Diabetes
Type 1 diabetes is characterized by autoimmune-mediated destruction of pancreatic β cells, with environmental factors potentially triggering this process in genetically susceptible individuals. Despite many not having a family history, certain genes increase susceptibility, suggesting a...
Diabetes Insipidus II: Pathophysiology

