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Laboratory for Retinal Cell Biology, Department Ophthalmology, Center for Integrative Human Physiology (CIHP) and Neuroscience Center Zurich (ZNZ), University Hospital, Zürich, Switzerland
1Correspondence: Laboratory for Retinal Cell Biology, Department Ophthalmology, University Hospital, Frauenklinikstrasse 24, 8091 Zürich, Switzerland. E-mail: cgrimm{at}opht.unizh.ch
ABSTRACT
Retinal degeneration is a major cause of severe visual impairment or blindness. Understanding the underlying molecular mechanisms is a prerequisite to develop therapeutic approaches for human patients. We show in three mouse models that induced and inherited retinal degeneration induces LIF and CLC as members of the interleukin (IL)-6 family of proteins, activates proteins of the Jak-STAT signaling pathway, and up-regulates suppressors of cytokine signaling as a negative feedback loop. Inhibition of Jak2 leads to protection of photoreceptors in a model of induced but not in a model of inherited retinal degeneration. Differential activation of Akt suggests alternative pathways for cell death and/or survival in different models. Proteins induced during photoreceptor degeneration are not mainly expressed in photoreceptors but in cells of other retinal layers. This suggests a model in which photoreceptor injury is signaled to cells of the inner retina, which in turn initiate a response either to support viability or accelerate death of injured cells.—Samardzija, M., Wenzel, A., Aufenberg, S., Thiersch, M., Remé, C., Grimm, C. Differential role of Jak-STAT signaling in retinal degenerations.
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