Newsportal - Ruhr-Universität Bochum
With their experiments the researchers gained new insights into the interplay of the extracellular protein tenascin-C and glaucoma.
A part of the research team: Jacqueline Reinhard, Andreas Faissner, Susanne Wiemann and Stephanie Joachim (from left)
The link between glaucoma, the immune system and protein tenascin-C
Researchers at Ruhr-Universität Bochum (RUB) have studied the role of the immune response in the development of glaucoma in mice. They showed that inflammatory processes are associated with the pathogenesis of the disease and that the extracellular matrix molecule tenascin-C plays a key role as a modulator of the immune response. Glaucoma is a common cause of blindness worldwide. Typically, intraocular pressure is increased in patients, but in around 40 per cent it stays in normal ranges. The results on the role of the immune response were published online on 9 October 2020 in the journal Frontiers in Immunology.
The collaborative study was carried out by Dr. Susanne Wiemann, Dr. Jacqueline Reinhard and Professor Andreas Faissner from the RUB Department of Cell Morphology and Molecular Neurobiology together with Dr. Sabrina Reinehr and Professor Stephanie Joachim from the Experimental Eye Research Institute at the University Eye Hospital in Bochum.
Tenascin-C affects the inflammatory immune response
The researchers studied mice that lacked tenascin-C and compared them with animals that exhibit this protein. In animals from both groups, they induced an autoimmune glaucoma, which is similar to glaucoma in humans.
In mice without tenascin-C, immune cells of the central nervous system, the microglia, behaved differently than in mice with tenascin-C. The cells were less reactive and released more anti-inflammatory factors. In animals with tenascin-C, however, the microglia secreted more pro-inflammatory factors.
Increased retinal cell death
The team also observed effects on retinal ganglion cells, which transmit visual information from the eye to the brain and typically die as a result of glaucomatous damage. In mice with tenascin-C, significantly more retinal ganglion cells died than in mice without tenascin-C. In contrast to mice with tenascin-C, the optic nerve remained intact in mice without tenascin-C.
The results suggest that tenascin-C plays a role in glaucoma by regulating inflammatory processes. “One day, this discovery could help in the early glaucoma diagnosis,” says Susanne Wiemann.
Susanne Wiemann was supported by a PhD grant from Konrad-Adenauer-Stiftung. The German Research Foundation financed the study as part of the FA 159/24-1 project.
Susanne Wiemann, Jacqueline Reinhard, Sabrina Reinehr, Zülal Cibir, Stephanie C. Joachim, Andreas Faissner: Loss of the extracellular matrix molecule Tenascin-C leads to absence of reactive gliosis and promotes anti-inflammatory cytokine expression in an autoimmune glaucoma mouse model, in: Frontiers in Immunology, 2020, DOI: 10.3389/fimmu.2020.566279
Prof. Dr. Andreas Faissner
Department of Cell Morphology and Molecular Neurobiology
Faculty of Biology and Biotechnology
Phone: +49 234 32 23851
Prof. Dr. Stephanie Joachim
Head of the Experimental Eye Research Institute
Phone: +49 234 299 3156
29 October 2020