Complement component 1q (C1q) is upregulated in the retina in murine and primate glaucoma

Abstract

Abstract: : Purpose: To determine whether C1q participates in the retinal pathophysiology associated with murine and primate glaucoma. Method: Young pre–pathologic (3 month old) and aged (15 month old) DBA2 mice with glaucomatous retinal pathology were used. Retinas were removed and subjected to Western blot analysis. Additionally other eyes were fixed and subjected to immunohistochemical analysis. C1q immunoreactivity was compared between eyes of young (pre–pathologic) and aged animals. In addition, sections from both eyes retinas from cynomolgus monkeys with experimental glaucoma in one eye were compared for C1q immunoreactivity. Results: Aged glaucomatous DBA2 mice with retinal pathology exhibited a marked increase in C1q immunoreactivity by Western blotting compared to young DBA2 mice. Most of the immunoreactive protein was localized by immunohistochemistry in the inner retina in a pattern consistent with its presence in the Müller cell layer. In addition, C1q immunoreactivity in the inner retina was upregulated in primate glaucomatous eyes compared to contralateral control eyes, and localized in a similar pattern. Conclusion: Retinal C1q is upregulated in both murine and primate experimental glaucoma. Upregulation of the first component of complement may indicate its participation in the retinal pathophysiology of this disease and reconfirms the relevance of the DBA2 strain as a model for the human disease.

Keywords: retinal degenerations: cell biology