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Traumatic brain injury increases levels of miR‐21 in extracellular vesicles: implications for neuroinflammation
Traumatic brain injury (TBI) is an important health concern and effective treatment strategies remain elusive. Understanding the complex multicellular response to TBI may provide new avenues for intervention. In the context of TBI, cell–cell communication is critical. One relatively unexplored form...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2016
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4971839/ https://www.ncbi.nlm.nih.gov/pubmed/27516962 http://dx.doi.org/10.1002/2211-5463.12092 |
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author | Harrison, Emily B. Hochfelder, Colleen G. Lamberty, Benjamin G. Meays, Brittney M. Morsey, Brenda M. Kelso, Matthew L. Fox, Howard S. Yelamanchili, Sowmya V. |
author_facet | Harrison, Emily B. Hochfelder, Colleen G. Lamberty, Benjamin G. Meays, Brittney M. Morsey, Brenda M. Kelso, Matthew L. Fox, Howard S. Yelamanchili, Sowmya V. |
author_sort | Harrison, Emily B. |
collection | PubMed |
description | Traumatic brain injury (TBI) is an important health concern and effective treatment strategies remain elusive. Understanding the complex multicellular response to TBI may provide new avenues for intervention. In the context of TBI, cell–cell communication is critical. One relatively unexplored form of cell–cell communication in TBI is extracellular vesicles (EVs). These membrane‐bound vesicles can carry many different types of cargo between cells. Recently, miRNA in EVs have been shown to mediate neuroinflammation and neuronal injury. To explore the role of EV‐associated miRNA in TBI, we isolated EVs from the brain of injured mice and controls, purified RNA from brain EVs, and performed miRNA sequencing. We found that the expression of miR‐212 decreased, while miR‐21, miR‐146, miR‐7a, and miR‐7b were significantly increased with injury, with miR‐21 showing the largest change between conditions. The expression of miR‐21 in the brain was primarily localized to neurons near the lesion site. Interestingly, adjacent to these miR‐21‐expressing neurons were activated microglia. The concurrent increase in miR‐21 in EVs with the elevation of miR‐21 in neurons, suggests that miR‐21 is secreted from neurons as potential EV cargo. Thus, this study reveals a new potential mechanism of cell–cell communication not previously described in TBI. |
format | Online Article Text |
id | pubmed-4971839 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-49718392016-08-11 Traumatic brain injury increases levels of miR‐21 in extracellular vesicles: implications for neuroinflammation Harrison, Emily B. Hochfelder, Colleen G. Lamberty, Benjamin G. Meays, Brittney M. Morsey, Brenda M. Kelso, Matthew L. Fox, Howard S. Yelamanchili, Sowmya V. FEBS Open Bio Research Articles Traumatic brain injury (TBI) is an important health concern and effective treatment strategies remain elusive. Understanding the complex multicellular response to TBI may provide new avenues for intervention. In the context of TBI, cell–cell communication is critical. One relatively unexplored form of cell–cell communication in TBI is extracellular vesicles (EVs). These membrane‐bound vesicles can carry many different types of cargo between cells. Recently, miRNA in EVs have been shown to mediate neuroinflammation and neuronal injury. To explore the role of EV‐associated miRNA in TBI, we isolated EVs from the brain of injured mice and controls, purified RNA from brain EVs, and performed miRNA sequencing. We found that the expression of miR‐212 decreased, while miR‐21, miR‐146, miR‐7a, and miR‐7b were significantly increased with injury, with miR‐21 showing the largest change between conditions. The expression of miR‐21 in the brain was primarily localized to neurons near the lesion site. Interestingly, adjacent to these miR‐21‐expressing neurons were activated microglia. The concurrent increase in miR‐21 in EVs with the elevation of miR‐21 in neurons, suggests that miR‐21 is secreted from neurons as potential EV cargo. Thus, this study reveals a new potential mechanism of cell–cell communication not previously described in TBI. John Wiley and Sons Inc. 2016-06-14 /pmc/articles/PMC4971839/ /pubmed/27516962 http://dx.doi.org/10.1002/2211-5463.12092 Text en © 2016 The Authors. Published by FEBS Press and John Wiley & Sons Ltd. This is an open access article under the terms of the Creative Commons Attribution (http://creativecommons.org/licenses/by/4.0/) License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Research Articles Harrison, Emily B. Hochfelder, Colleen G. Lamberty, Benjamin G. Meays, Brittney M. Morsey, Brenda M. Kelso, Matthew L. Fox, Howard S. Yelamanchili, Sowmya V. Traumatic brain injury increases levels of miR‐21 in extracellular vesicles: implications for neuroinflammation |
title | Traumatic brain injury increases levels of miR‐21 in extracellular vesicles: implications for neuroinflammation |
title_full | Traumatic brain injury increases levels of miR‐21 in extracellular vesicles: implications for neuroinflammation |
title_fullStr | Traumatic brain injury increases levels of miR‐21 in extracellular vesicles: implications for neuroinflammation |
title_full_unstemmed | Traumatic brain injury increases levels of miR‐21 in extracellular vesicles: implications for neuroinflammation |
title_short | Traumatic brain injury increases levels of miR‐21 in extracellular vesicles: implications for neuroinflammation |
title_sort | traumatic brain injury increases levels of mir‐21 in extracellular vesicles: implications for neuroinflammation |
topic | Research Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4971839/ https://www.ncbi.nlm.nih.gov/pubmed/27516962 http://dx.doi.org/10.1002/2211-5463.12092 |
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