PT  - JOURNAL ARTICLE
AU  - Diana Pauly
AU  - Nicole Schäfer
AU  - Felix Grassmann
AU  - Anna M. Pfaller
AU  - Tobias Straub
AU  - Bernhard H. F. Weber
AU  - Stefanie M. Hauck
AU  - Antje Grosche
TI  - Cell type-specific complement expression from healthy and diseased retinae
AID  - 10.1101/413088
DP  - 2018 Jan 01
TA  - bioRxiv
PG  - 413088
4099  - http://biorxiv.org/content/early/2018/09/10/413088.short
4100  - http://biorxiv.org/content/early/2018/09/10/413088.full
AB  - Retinal degeneration is associated with complement system activation, but retinal sources of complement are unknown. Here, we describe the human and murine complement transcriptomes of Müller cells, microglia/macrophages, vascular cells, neurons and retinal pigment epithelium (RPE) in health and disease. All cell populations expressed c1s, c3, cfb, cfp, cfh and cfi. Murine Müller cells contributed the highest amount of complement activators (c1s, c3, cfb). RPE mainly expressed cfh, while cfi and cfp transcripts were most abundant in neurons. The main complement negative regulator in the human retina was cfi, while cfh dominated in the murine retina. Importantly, the expression of c1s, cfb, cfp, cfi increased and that of cfh decreased with aging. Impaired photoreceptor recycling led to an enhanced c3 expression in RPE and to a reduced cfi expression in microglia/macrophages. Expression of complement components was massively upregulated after transient retinal ischemia in murine microglia, Müller cells and RPE. The individual signature of complement expression in distinct murine and human retinal cell types indicates a local, well-orchestrated regulation of the complement system in both species.