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1 General aspects (0)   1.1 Epidemiology (6)   1.2 Population genetics (4)   1.3 Pathogenesis (8)   1.4 Quality of life (5)   1.5 Glaucomas as cause of blindness (4)   1.6 Prevention and screening (9) 2 Anatomical structures in glaucoma (0)   2.1 Conjunctiva (3)   2.2 Cornea (19)   2.3 Sclera (2)   2.4 Anterior chamber angle (6)   2.5 Meshwork (0)     2.5.1 Trabecular meshwork (10)     2.5.2 Schlemms canal (2)     2.5.3 Scleral outlet channels (1)   2.6 Aqueous humor dynamics (1)     2.6.1 Production (1)     2.6.2 Outflow (1)       2.6.2.1 Trabecular meshwork (3)       2.6.2.2 Uveoscleral (0)     2.6.3 Compostion (6)   2.7 Episcleral veins and venous pressure (0)   2.8 Iris (0)   2.9 Ciliary body (2)   2.10 Lens (0)   2.11 Vitreous body (0)   2.12 Choroid, peripapillary choroid, peripapillary atrophy (4)   2.13 Retina and retinal nerve fibre layer (23)   2.14 Optic disc (20)   2.15 Optic nerve (2)   2.16 Chiasma and retrochiasmal central nervous system (4)   2.17 Stem cells (4)   2.20 Other (0) 3 Laboratory methods (0)   3.1 Microscopy (1)   3.2 Electron microscopy (0)   3.3 Immunohistochemistry (2)   3.4 Molecular genetics (0)     3.4.1 Linkage studies (0)     3.4.2 Gene studies (29)   3.5 Molecular biology incl. 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Miscellaneous (19)

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Abstract #26048 Published in IGR 12-2

Modulation of morphological changes of microglia and neuroprotection by monocyte chemoattractant protein-1 in experimental glaucoma

Chiu K; Yeung SC; So KF; Chang RC
Cellular and Molecular Immunology 2010; 7: 61-68

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Monocyte chemoattractant protein-1 (MCP-1)/CCL2 is a C-C chemokine involved in the activation and recruitment of monocytic cells to injury sites. MCP-1/CCL2 can induce either neuroprotection or neurodestruction in vitro, depending on the experimental model. We aim to use MCP-1/CCL2 as an experimental tool to investigate the morphological changes of microglia when loss of healthy retinal ganglion cells (RGCs) is exacerbated or attenuated in an experimental glaucoma model. While a high concentration (1000 ng) of MCP-1/CCL2 and lipopolysaccharide (LPS)-exacerbated RGC loss, 100 ng MCP-1/CCL2 provided neuroprotection towards RGC. Neuroprotective MCP-1/CCL2 (100 ng) also upregulated insulin-like growth factor-1 (IGF-1) immunoreactivity in the RGCs. The neuroprotective effect of MCP-1/CCL2 was not due to the massive infiltration of microglia/macrophages. Taken together, this is the first report showing that an appropriate amount of MCP-1/CCL2 can protect RGCs in experimental glaucoma.

K. Chiu. Laboratory of Neurodegenerative Diseases, Department of Anatomy, University of Hong Kong, Pokfulam, Hong Kong, China.

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Classification:

11.8 Neuroprotection (Part of: 11 Medical treatment)
5 Experimental glaucoma; animal models
3.10 Immunobiology (Part of: 3 Laboratory methods)

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