Cross-talk between monocyte invasion and astrocyte proliferation regulates scarring in brain injury
Scar formation after brain injury is still poorly understood. To further elucidate such processes, here, we examine the interplay between astrocyte proliferation taking place predominantly at the vascular interface and monocyte invasion. Using genetic mouse models that decrease or increase reactive...
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Autores principales: | , , , , , , , , , |
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Formato: | Articulo |
Lenguaje: | Inglés |
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2018
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Acceso en línea: | http://sedici.unlp.edu.ar/handle/10915/118630 |
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I19-R120-10915-118630 |
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institution |
Universidad Nacional de La Plata |
institution_str |
I-19 |
repository_str |
R-120 |
collection |
SEDICI (UNLP) |
language |
Inglés |
topic |
Biología aryl hydrocarbon receptor astrogliosis monocytes scar formation sonic hedgehog pathway traumatic brain injury |
spellingShingle |
Biología aryl hydrocarbon receptor astrogliosis monocytes scar formation sonic hedgehog pathway traumatic brain injury Frik, Jesica Merl-Pham, Juliane Plesnila, Nikolaus Mattugini, Nicola Kjell, Jacob Kraska, Jonas Gómez, Ricardo Martín Hauck, Stefanie M. Sirko, Swetlana Götz, Magdalena Cross-talk between monocyte invasion and astrocyte proliferation regulates scarring in brain injury |
topic_facet |
Biología aryl hydrocarbon receptor astrogliosis monocytes scar formation sonic hedgehog pathway traumatic brain injury |
description |
Scar formation after brain injury is still poorly understood. To further elucidate such processes, here, we examine the interplay between astrocyte proliferation taking place predominantly at the vascular interface and monocyte invasion. Using genetic mouse models that decrease or increase reactive astrocyte proliferation, we demonstrate inverse effects on monocyte numbers in the injury site. Conversely, reducing monocyte invasion using CCR2-/- mice causes a strong increase in astrocyte proliferation, demonstrating an intriguing negative cross-regulation between these cell types at the vascular interface. CCR2-/- mice show reduced scar formation with less extracellular matrix deposition, smaller lesion site and increased neuronal coverage. Surprisingly, the GFAP+ scar area in these mice is also significantly decreased despite increased astrocyte proliferation. Proteomic analysis at the peak of increased astrocyte proliferation reveals a decrease in extracellular matrix synthesizing enzymes in the injury sites of CCR2-/- mice, highlighting how early key aspects of scar formation are initiated. Taken together, we provide novel insights into the cross-regulation of juxtavascular proliferating astrocytes and invading monocytes as a crucial mechanism of scar formation upon brain injury. |
format |
Articulo Articulo |
author |
Frik, Jesica Merl-Pham, Juliane Plesnila, Nikolaus Mattugini, Nicola Kjell, Jacob Kraska, Jonas Gómez, Ricardo Martín Hauck, Stefanie M. Sirko, Swetlana Götz, Magdalena |
author_facet |
Frik, Jesica Merl-Pham, Juliane Plesnila, Nikolaus Mattugini, Nicola Kjell, Jacob Kraska, Jonas Gómez, Ricardo Martín Hauck, Stefanie M. Sirko, Swetlana Götz, Magdalena |
author_sort |
Frik, Jesica |
title |
Cross-talk between monocyte invasion and astrocyte proliferation regulates scarring in brain injury |
title_short |
Cross-talk between monocyte invasion and astrocyte proliferation regulates scarring in brain injury |
title_full |
Cross-talk between monocyte invasion and astrocyte proliferation regulates scarring in brain injury |
title_fullStr |
Cross-talk between monocyte invasion and astrocyte proliferation regulates scarring in brain injury |
title_full_unstemmed |
Cross-talk between monocyte invasion and astrocyte proliferation regulates scarring in brain injury |
title_sort |
cross-talk between monocyte invasion and astrocyte proliferation regulates scarring in brain injury |
publishDate |
2018 |
url |
http://sedici.unlp.edu.ar/handle/10915/118630 |
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bdutipo_str |
Repositorios |
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