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: Frik, Jesica, Merl-Pham, Juliane, Plesnila, Nikolaus, Mattugini, Nicola, Kjell, Jacob, Kraska, Jonas, Gómez, Ricardo Martín, Hauck, Stefanie M., Sirko, Swetlana, Götz, Magdalena
Formato: Articulo
Lenguaje:Inglés
Publicado: 2018
Materias:
Acceso en línea:http://sedici.unlp.edu.ar/handle/10915/118630
Aporte de:
id I19-R120-10915-118630
record_format dspace
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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