Acute intranasal osteopontin treatment in male rats following TBI increases the number of activated microglia but does not alter lesion characteristics
| Autor: | Jiping Tang, Richard E. Hartman, Mary Hamer, William J. Pearce, Amandine Jullienne, Elizabeth Haddad, Alexander Morita, Andre Obenaus, John H. Zhang, Peter Gifford |
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| Rok vydání: | 2019 |
| Předmět: |
Male
0301 basic medicine Pathology medicine.medical_specialty Traumatic brain injury Brain Edema Neuroprotection Article Rats Sprague-Dawley Lesion 03 medical and health sciences Cellular and Molecular Neuroscience 0302 clinical medicine stomatognathic system Edema Brain Injuries Traumatic medicine Animals Osteopontin Acquired brain injury Neuroinflammation Microglia biology business.industry Brain medicine.disease Rats Disease Models Animal Neuroprotective Agents 030104 developmental biology medicine.anatomical_structure Blood-Brain Barrier biology.protein medicine.symptom business 030217 neurology & neurosurgery Signal Transduction |
| Zdroj: | J Neurosci Res |
| ISSN: | 1097-4547 0360-4012 |
| Popis: | Intranasal recombinant osteopontin (OPN) has been shown to be neuroprotective in different models of acquired brain injury but has never been tested after traumatic brain injury (TBI). We used a model of moderate-to-severe controlled cortical impact in male adult Sprague-Dawley rats and tested our hypothesis that OPN treatment would improve neurological outcomes, lesion and brain tissue characteristics, neuroinflammation, and vascular characteristics at one day post-injury. Intranasal OPN administered one hour after the TBI did not improve neurological score, lesion volumes, blood-brain barrier or vascular characteristics. When assessing neuroinflammation, we did not observe any effect of OPN on the astrocyte reactivity but discovered an increased number of activated microglia within the ipsilateral hemisphere. Moreover, we found a correlation between edema and heme oxygenase-1 (HO-1) expression which was decreased in OPN-treated animals, suggesting an effect of OPN on the HO-1 response to injury. Thus, OPN may increase or accelerate the microglial response after TBI, and early response of HO-1 in modulating edema formation may limit the secondary consequences of TBI at later time points. Additional experiments and at longer time points are needed to determine if intranasal OPN could potentially be used as a treatment after TBI where it might be beneficial by activating protective signaling pathways. |
| Databáze: | OpenAIRE |
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