The effect of osteopontin and osteopontin-derived peptides on preterm brain injury
BACKGROUND: Osteopontin (OPN) is a highly phosphorylated sialoprotein and a soluble cytokine that is widely expressed in a variety of tissues, including the brain. OPN and OPN-derived peptides have been suggested to have potential neuroprotective effects against ischemic brain injury, but their role...
Autores principales: | , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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BioMed Central
2014
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4266908/ https://www.ncbi.nlm.nih.gov/pubmed/25465048 http://dx.doi.org/10.1186/s12974-014-0197-0 |
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author | Albertsson, Anna-Maj Zhang, Xiaoli Leavenworth, Jianmei Bi, Dan Nair, Syam Qiao, Lili Hagberg, Henrik Mallard, Carina Cantor, Harvey Wang, Xiaoyang |
author_facet | Albertsson, Anna-Maj Zhang, Xiaoli Leavenworth, Jianmei Bi, Dan Nair, Syam Qiao, Lili Hagberg, Henrik Mallard, Carina Cantor, Harvey Wang, Xiaoyang |
author_sort | Albertsson, Anna-Maj |
collection | PubMed |
description | BACKGROUND: Osteopontin (OPN) is a highly phosphorylated sialoprotein and a soluble cytokine that is widely expressed in a variety of tissues, including the brain. OPN and OPN-derived peptides have been suggested to have potential neuroprotective effects against ischemic brain injury, but their role in preterm brain injury is unknown. METHODS: We used a hypoxia-ischemia (HI)-induced preterm brain injury model in postnatal day 5 mice. OPN and OPN-derived peptides were given intracerebroventricularly and intranasally before HI. Brain injury was evaluated at 7 days after the insults. RESULTS: There was a significant increase in endogenous OPN mRNA and OPN protein in the mouse brain after the induction of HI at postnatal day 5. Administration of full-length OPN protein and thrombin-cleaved OPN did not affect preterm brain injury. This was demonstrated with both intracerebroventricular and intranasal administration of OPN as well as in OPN-deficient mice. Interestingly, both N134–153 and C154–198 OPN-derived peptides increased the severity of brain injury in this HI-induced preterm brain injury model. CONCLUSIONS: The neuroprotective effects of OPN are age-dependent, and, in contrast to the more mature brain, OPN-derived peptides potentiate injury in postnatal day 5 mice. Intranasal administration is an efficient way of delivering drugs to the central nervous system (CNS) in neonatal mice and is likely to be an easy and noninvasive method of drug delivery to the CNS in preterm infants. |
format | Online Article Text |
id | pubmed-4266908 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2014 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-42669082014-12-16 The effect of osteopontin and osteopontin-derived peptides on preterm brain injury Albertsson, Anna-Maj Zhang, Xiaoli Leavenworth, Jianmei Bi, Dan Nair, Syam Qiao, Lili Hagberg, Henrik Mallard, Carina Cantor, Harvey Wang, Xiaoyang J Neuroinflammation Research BACKGROUND: Osteopontin (OPN) is a highly phosphorylated sialoprotein and a soluble cytokine that is widely expressed in a variety of tissues, including the brain. OPN and OPN-derived peptides have been suggested to have potential neuroprotective effects against ischemic brain injury, but their role in preterm brain injury is unknown. METHODS: We used a hypoxia-ischemia (HI)-induced preterm brain injury model in postnatal day 5 mice. OPN and OPN-derived peptides were given intracerebroventricularly and intranasally before HI. Brain injury was evaluated at 7 days after the insults. RESULTS: There was a significant increase in endogenous OPN mRNA and OPN protein in the mouse brain after the induction of HI at postnatal day 5. Administration of full-length OPN protein and thrombin-cleaved OPN did not affect preterm brain injury. This was demonstrated with both intracerebroventricular and intranasal administration of OPN as well as in OPN-deficient mice. Interestingly, both N134–153 and C154–198 OPN-derived peptides increased the severity of brain injury in this HI-induced preterm brain injury model. CONCLUSIONS: The neuroprotective effects of OPN are age-dependent, and, in contrast to the more mature brain, OPN-derived peptides potentiate injury in postnatal day 5 mice. Intranasal administration is an efficient way of delivering drugs to the central nervous system (CNS) in neonatal mice and is likely to be an easy and noninvasive method of drug delivery to the CNS in preterm infants. BioMed Central 2014-12-03 /pmc/articles/PMC4266908/ /pubmed/25465048 http://dx.doi.org/10.1186/s12974-014-0197-0 Text en © Albertsson et al.; licensee BioMed Central Ltd. 2014 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated. |
spellingShingle | Research Albertsson, Anna-Maj Zhang, Xiaoli Leavenworth, Jianmei Bi, Dan Nair, Syam Qiao, Lili Hagberg, Henrik Mallard, Carina Cantor, Harvey Wang, Xiaoyang The effect of osteopontin and osteopontin-derived peptides on preterm brain injury |
title | The effect of osteopontin and osteopontin-derived peptides on preterm brain injury |
title_full | The effect of osteopontin and osteopontin-derived peptides on preterm brain injury |
title_fullStr | The effect of osteopontin and osteopontin-derived peptides on preterm brain injury |
title_full_unstemmed | The effect of osteopontin and osteopontin-derived peptides on preterm brain injury |
title_short | The effect of osteopontin and osteopontin-derived peptides on preterm brain injury |
title_sort | effect of osteopontin and osteopontin-derived peptides on preterm brain injury |
topic | Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4266908/ https://www.ncbi.nlm.nih.gov/pubmed/25465048 http://dx.doi.org/10.1186/s12974-014-0197-0 |
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