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Expression of glutamine synthetase and cell proliferation in human idiopathic epiretinal membrane
1Department of Ophthalmology and Visual Sciences, Hokkaido University Graduate School of Medicine, Kita-ku, Sapporo 060-8638, Japan. kaseron@med.hokudai.ac.jp
Background/Aim:
The mechanisms of the cellular origin and cell proliferation in the idiopathic epiretinal membrane (ERM) are unsolved. The aim of this study was to examine the expression of cell cycle related molecules and glutamine synthetase (GS), which is expressed in Müller cells and their processes, in ERM tissues.
Methods:
The ERMs were surgically removed using pars plana vitrectomy. Formalin fixed, paraffin embedded ERM tissues were analysed by immunohistochemistry with anti-cyclin D1, p27 (KIP1), proliferating cell nuclear antigen (PCNA), and GS antibodies.
Results:
The histopathological findings showed that all the ERMs consisted of oval or spindle mononuclear cells with thin collagen-like tissues. Immunoreactivity for GS was detected in collagen-like tissues of ERM, presenting a continuous, isodense pattern. GS immunopositive cells in all cases expressed PCNA in their nuclei. Nuclear immunoreactivity for cyclin D1 was noted in the ERM constituent cells, whereas p27 (KIP1) positive nuclei were not detected.
Conclusion:
Cyclin D1 and PCNA were expressed in the idiopathic ERM, which was mainly derived from Müller cells and extensions of their processes.
Insights
Idiopathic epiretinal membranes (ERM) involve Müller cells expressing cell cycle markers like cyclin D1 and proliferating cell nuclear antigen (PCNA). These findings suggest Müller cell proliferation contributes to ERM formation.
Area of Science:
- Ophthalmology
- Cell Biology
- Retinal Diseases
Background:
- The cellular origin and proliferation mechanisms of idiopathic epiretinal membrane (ERM) remain unclear.
- Müller cells are implicated in ERM pathogenesis, expressing glutamine synthetase (GS).
Purpose of the Study:
- To investigate cell cycle-related molecules and glutamine synthetase (GS) expression in ERM tissues.
- To elucidate the cellular origin and proliferation processes in idiopathic ERM.
Main Methods:
- Surgical removal of ERM tissues via pars plana vitrectomy.
- Immunohistochemical analysis of ERM tissues using antibodies for cyclin D1, p27 (KIP1), proliferating cell nuclear antigen (PCNA), and GS.
Main Results:
- ERM tissues comprised mononuclear cells and collagen-like tissues with GS immunoreactivity.
- GS-positive cells in ERM showed nuclear PCNA expression, indicating proliferation.
- Cyclin D1 was detected in ERM cells, while p27 (KIP1) was not found.
Conclusions:
- Idiopathic ERM exhibits expression of cyclin D1 and PCNA.
- These findings suggest that idiopathic ERM is primarily derived from Müller cells and their processes.
