Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
3063818 | Journal of Neuroimmunology | 2016 | 13 Pages |
•In an in vitro model of retinal degeneration, C1q supplementation increases ganglion cell survival.•The endogenous C1q production of the degenerating retina was suppressed by C1q supplementation.•The addition of C1q attenuated the gliotic response.
Using a previously described retinal explant culture system as an acute injury model, we here explore the role of C1q, the initiator of the classical complement pathway, in neuronal cell survival and retinal homeostasis.Full-thickness adult rat retinal explants were divided into four groups, receiving the following supplementation: C1q (50 nM), C1-inhibitor (C1-inh; Berinert; 500 mg/l), C1q + C1-inh, and no supplementation (culture controls). Explants were kept for 12 h or 2 days after which they were examined morphologically and with a panel of immunohistochemical markers.C1q supplementation protects ganglion cells from degeneration within the explant in vitro system. This effect is correlated to an attenuated endogenous production of C1q, and a quiesced gliotic response.