Astrogliosis is delayed in type 1 interleukin-1 receptor-null mice following a penetrating brain injury |
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Authors: | Hsiao-Wen Lin Anirban Basu Charles Druckman Michael Cicchese J Kyle Krady Steven W Levison |
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Institution: | (1) Department of Neurology and Neuroscience, UMDNJ-New Jersey Medical School, Newark, NJ 07103, USA;(2) National Brain Research Centre, Gurgaon, 122 050, India;(3) Dept. of Neural and Behavioral Sciences, The Pennsylvania State University College of Medicine, Hershey, PA 17033, USA |
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Abstract: | The cytokines IL-1α and IL-1β are induced rapidly after insults to the CNS, and their subsequent signaling through the type
1 IL-1 receptor (IL-1R1) has been regarded as essential for a normal astroglial and microglial/macrophage response. To determine
whether abrogating signaling through the IL-1R1 will alter the cardinal astrocytic responses to injury, we analyzed molecules
characteristic of activated astrocytes in response to a penetrating stab wound in wild type mice and mice with a targeted
deletion of IL-1R1. Here we show that after a stab wound injury, glial fibrillary acidic protein (GFAP) induction on a per
cell basis is delayed in the IL-1R1-null mice compared to wild type counterparts. However, the induction of chondroitin sulfate
proteoglycans, tenascin, S-100B as well as glutamate transporter proteins, GLAST and GLT-1, and glutamine synthetase are independent
of IL-1RI signaling. Cumulatively, our studies on gliosis in the IL-1R1-null mice indicate that abrogating IL-1R1 signaling
delays some responses of astroglial activation; however, many of the important neuroprotective adaptations of astrocytes to
brain trauma are preserved. These data recommend the continued development of therapeutics to abrogate IL-1R1 signaling to
treat traumatic brain injuries. However, astroglial scar related proteins were induced irrespective of blocking IL-1R1 signaling
and thus, other therapeutic strategies will be required to inhibit glial scarring. |
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