Kaczmarek-Hajek, Karina and Zhang, Jiong and Kopp, Robin and Grosche, Antje and Rissiek, Bjoern and Saul, Anika and Bruzzone, Santina and Engel, Tobias and Jooss, Tina and Krautloher, Anna and Schuster, Stefanie and Magnus, Tim and Stadelmann, Christine and Sirko, Swetlana and Koch-Nolte, Friedrich and Eulenburg, Volker and Nicke, Annette (2018) Re-evaluation of neuronal P2X7 expression using novel mouse models and a P2X7-specific nanobody. ELIFE, 7: e36217. ISSN 2050-084X,
Full text not available from this repository. (Request a copy)Abstract
The P2X7 channel is involved in the pathogenesis of various CNS diseases. An increasing number of studies suggest its presence in neurons where its putative functions remain controversial for more than a decade. To resolve this issue and to provide a model for analysis of P2X7 functions, we generated P2X7 BAC transgenic mice that allow visualization of functional EGFP-tagged P2X7 receptors in vivo. Extensive characterization of these mice revealed dominant P2X7-EGFP protein expression in microglia, Bergmann glia, and oligodendrocytes, but not in neurons. These findings were further validated by microglia- and oligodendrocyte-specific P2X7 deletion and a novel P2X7-specific nanobody. In addition to the first quantitative analysis of P2X7 protein expression in the CNS, we show potential consequences of its overexpression in ischemic retina and post-traumatic cerebral cortex grey matter. This novel mouse model overcomes previous limitations in P2X7 research and will help to determine its physiological roles and contribution to diseases.
| Item Type: | Article |
|---|---|
| Uncontrolled Keywords: | RECEPTOR-MESSENGER-RNA; MULLER GLIAL-CELLS; P2X(7) RECEPTORS; CEREBRAL-CORTEX; STATUS EPILEPTICUS; CMT1A NEUROPATHY; GENE-EXPRESSION; MICE; RETINA; PORE; |
| Subjects: | 600 Technology > 610 Medical sciences Medicine |
| Divisions: | Medicine > Lehrstuhl für Humangenetik |
| Depositing User: | Dr. Gernot Deinzer |
| Date Deposited: | 05 Mar 2020 10:12 |
| Last Modified: | 05 Mar 2020 10:12 |
| URI: | https://pred.uni-regensburg.de/id/eprint/14062 |
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