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Astrocytic expression of the CXCL12 receptor, CXCR7/ACKR3 is a hallmark of the diseased, but not developing CNS
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Puchert, Malte, Pelkner, Fabian, Stein, Gregor, Angelov, Doychin N., Boltze, Johannes, Wagner, Daniel-Christoph, Odoardi, Francesca, Flügel, Alexander, Streit, Wolfgang J. and Engele, Jürgen (2017) Astrocytic expression of the CXCL12 receptor, CXCR7/ACKR3 is a hallmark of the diseased, but not developing CNS. Molecular and Cellular Neuroscience, 85 . pp. 105-118. doi:10.1016/j.mcn.2017.09.001 ISSN 1044-7431.
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Official URL: http://dx.doi.org/10.1016/j.mcn.2017.09.001
Abstract
Based on our previous demonstration of CXCR7 as the major mediator of CXCL12 signaling in cultured astrocytes, we have now compared astrocytic expression of the CXCL12 receptors, CXCR7 and CXCR4, during CNS development and disease. In addition, we asked whether disease-associated conditions/factors affect expression of CXCL12 receptors in astrocytes. In the late embryonic rat brain, CXCR7+/GFAP+ cells were restricted to the ventricular/subventricular zone while CXCR4 was widely absent from GFAP-positive cells. In the early postnatal and adult brain, CXCR7 and CXCR4 were almost exclusively expressed by GFAP-immunoreactive astrocytes forming the superficial glia limitans. Contrasting the situation in the intact CNS, a striking increase in astrocytic CXCR7 expression was detectable in the cortex of rats with experimental brain infarcts, in the spinal cord of rats with experimental autoimmune encephalomyelitis (EAE) and after mechanical compression, as well as in the in infarcted human cerebral cortex and in the hippocampus of Alzheimer's disease patients. None of these pathologies was associated with substantial increases in astrocytic CXCR4 expression. Screening of various disease-associated factors/conditions further revealed that CXCR7 expression of cultured cortical astrocytes increases with IFNγ as well as under hypoxic conditions whereas CXCR7 expression is attenuated following treatment with IFNβ. Again, none of the treatments affected CXCR4 expression in cultured astrocytes. Together, these findings support the hypothesis of a crucial role of astrocytic CXCR7 in the progression of various CNS pathologies.
| Item Type: | Journal Article | ||||||||
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| Divisions: | Faculty of Science, Engineering and Medicine > Science > Life Sciences (2010- ) | ||||||||
| Journal or Publication Title: | Molecular and Cellular Neuroscience | ||||||||
| Publisher: | Elsevier | ||||||||
| ISSN: | 1044-7431 | ||||||||
| Official Date: | December 2017 | ||||||||
| Dates: |
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| Volume: | 85 | ||||||||
| Page Range: | pp. 105-118 | ||||||||
| DOI: | 10.1016/j.mcn.2017.09.001 | ||||||||
| Status: | Peer Reviewed | ||||||||
| Publication Status: | Published | ||||||||
| Access rights to Published version: | Restricted or Subscription Access |
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