Abstract Title

C1q induction and glial activation following optic nerve injury

Presenter Name

Elliott M. Allums

RAD Assignment Number

1001

Abstract

Purpose: Complement protein 1 subunit q (C1q) is a component of the C1 complex of the classical pathway of complement activation. It plays a role in synaptic development and pruning of central nervous system, as well as in the pathogenesis of various neurodegenerative diseases. In this study, we characterized C1q expression in C57BL/6J mice in an optic nerve crush (ONC) model of neurodegeneration. We also examined glial activation to determine possible sources of the increased C1q expression.

Methods: Acute injury was induced in adult C57BL/6J mice by intraorbital ONC performed approximately 1 mm posterior to the optic nerve head with self-closing forceps for four seconds. C1q expression and glial activation (GFAP) was determined at 3 and 7 days post ONC by immunohistochemistry (IHC) as well as Western Blotting.

Results: C1q expression increased in the crush site in the optic nerve, the inner plexiform layer (IPL) and the outer plexiform layer (OPL) of the retina 3 days after ONC. C1q expression further increased 7 days after ONC in the crush site, IPL, OPL, as well as the ganglion cell layer (GCL). Optic nerve injury increased glial fibrillary acidic protein (GFAP) expression in the GCL layer, extending through the retinal layers, 7 days post ONC and ED1 expression in the crush site 3 and 7 days following ONC.

Conclusions: This study shows that C1q may play a role in neurodegeneration and could have potential as a therapeutic target. Glial cells may be responsible for the increased expression in C1q following ONC.

Research Area

Eye/Vision

Presentation Type

Poster

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C1q induction and glial activation following optic nerve injury

Purpose: Complement protein 1 subunit q (C1q) is a component of the C1 complex of the classical pathway of complement activation. It plays a role in synaptic development and pruning of central nervous system, as well as in the pathogenesis of various neurodegenerative diseases. In this study, we characterized C1q expression in C57BL/6J mice in an optic nerve crush (ONC) model of neurodegeneration. We also examined glial activation to determine possible sources of the increased C1q expression.

Methods: Acute injury was induced in adult C57BL/6J mice by intraorbital ONC performed approximately 1 mm posterior to the optic nerve head with self-closing forceps for four seconds. C1q expression and glial activation (GFAP) was determined at 3 and 7 days post ONC by immunohistochemistry (IHC) as well as Western Blotting.

Results: C1q expression increased in the crush site in the optic nerve, the inner plexiform layer (IPL) and the outer plexiform layer (OPL) of the retina 3 days after ONC. C1q expression further increased 7 days after ONC in the crush site, IPL, OPL, as well as the ganglion cell layer (GCL). Optic nerve injury increased glial fibrillary acidic protein (GFAP) expression in the GCL layer, extending through the retinal layers, 7 days post ONC and ED1 expression in the crush site 3 and 7 days following ONC.

Conclusions: This study shows that C1q may play a role in neurodegeneration and could have potential as a therapeutic target. Glial cells may be responsible for the increased expression in C1q following ONC.