کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
5534421 1551121 2017 14 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Astrocytic expression of the CXCL12 receptor, CXCR7/ACKR3 is a hallmark of the diseased, but not developing CNS
موضوعات مرتبط
علوم زیستی و بیوفناوری بیوشیمی، ژنتیک و زیست شناسی مولکولی بیولوژی سلول
پیش نمایش صفحه اول مقاله
Astrocytic expression of the CXCL12 receptor, CXCR7/ACKR3 is a hallmark of the diseased, but not developing CNS
چکیده انگلیسی


- CXCR7 and CXCR4 are normally only present in astrocytes forming the glia limitans.
- In the diseased CNS, astrocytes prominently express CXCR7, but not CXCR4.
- IFNγ, IFNβ, and hypoxia modulate astrocytic expression of CXCR7, but not of CXCR4.

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.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Molecular and Cellular Neuroscience - Volume 85, December 2017, Pages 105-118
نویسندگان
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