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[Mononuclear phagocytes and their growth factors: pacemakers of proliferative vitreoretinopathy?]
M Weller1, K Heimann, P Wiedemann
1Abt. für Netzhaut- und Glaskörperchirurgie, Universitäts-Augenklinik Köln.
Abstract:
Recent studies on the natural course of proliferative vitreoretinopathy (PVR) have focused on the mononuclear phagocyte system (MPS). Although the precise origin of these cells is not known, current evidence indicates that peripheral blood monocytes infiltrate a lesion initially, subsequently giving way to resident phagocytic cells. In this context the authors try to clarify some aspects of the confusing nomenclature of phagocytic monocytes, macrophages, and microglia. The concept of the blood-retinal barrier (BRB) and its breakdown in PVR are presented and discussed. Platelet-derived growth factor (PDGF) and transforming growth factor-beta (TGF-beta), both secretory products of macrophages, have recently been implicated in the development of vitreoretinal pathology. These studies, however, are difficult to evaluate because the biological effects of different growth factors are closely interrelated and vary widely, including both inhibition as well as stimulation of cell growth. The authors hypothesize that plasma of macrophage-derived TGF-beta provokes an increase in fibronectin synthesis, which in turn is responsible for the fibrotic rebuilding of the vitreoretinal interface in PVR. As an adjunct to the pharmacological treatment of PVR with Daunomycin the use of steroids is recommended to suppress the initial macrophage activation and related dysfunction of the BRB.
Insights
Proliferative vitreoretinopathy (PVR) involves the mononuclear phagocyte system (MPS). Macrophage-derived TGF-beta may increase fibronectin, causing fibrotic rebuilding in PVR, suggesting steroids could help suppress macrophage activation.
Area of Science:
- Ophthalmology and immunology
- Cell biology and pathology
Context:
- Proliferative vitreoretinopathy (PVR) pathogenesis involves the mononuclear phagocyte system (MPS).
- The blood-retinal barrier (BRB) integrity and breakdown in PVR are critical areas of study.
- The nomenclature of phagocytic cells like monocytes, macrophages, and microglia requires clarification.
Purpose:
- To clarify the role of phagocytic cells in PVR.
- To discuss the blood-retinal barrier (BRB) breakdown in PVR.
- To explore the involvement of growth factors like PDGF and TGF-beta in vitreoretinal pathology.
Summary:
- Peripheral blood monocytes infiltrate PVR lesions, later replaced by resident phagocytes.
- Macrophage-derived transforming growth factor-beta (TGF-beta) may stimulate fibronectin synthesis, leading to fibrotic rebuilding of the vitreoretinal interface.
- Steroids are proposed as an adjunct to Daunomycin to inhibit initial macrophage activation and BRB dysfunction in PVR.
Impact:
- Provides a clearer understanding of PVR cellular mechanisms.
- Highlights the potential role of TGF-beta and fibronectin in PVR fibrosis.
- Suggests therapeutic strategies involving steroids to manage PVR by targeting macrophage activation and BRB integrity.