Fibronectin and laminin increase in the mouse brain after controlled cortical impact injury

Ciara C. Tate, Matthew C. Tate, Michelle C. LaPlaca*

*Corresponding author for this work

Research output: Contribution to journalArticle

35 Citations (Scopus)

Abstract

The complex environment of the traumatically injured brain exhibits aspects of inhibition and ongoing cell death together with attempts at repair and regeneration. Elucidating these events and exploiting those factors involved in endogenous repair and regeneration may aid in developing more effective treatments for traumatic brain injury. Two extracellular matrix proteins critical to neural development - fibronectin and laminin - may also play a protective or reparative role in the injury response. While both of these proteins have been found to increase following human brain injury, the presence of these proteins has not been studied in a clinically-relevant animal model of blunt head trauma. In this study, we examined the spatiotemporal profile of both fibronectin and laminin in the mouse brain following controlled cortical impact injury. Fibronectin and laminin reactivity was localized to the injury penumbra up to 14 days post-injury and was significantly higher than uninjured controls at 3 days post-injury. Upon examining the spatial relationship of fibronectin and laminin to support cells, we found macrophages/activated microglia prominently present in the fibronectin-rich tissue, consistent with a role for fibronectin in facilitating debris clearing. Furthermore, reactive astrocyte processes were found sheathing laminin positive vasculature, suggesting that laminin may play a role in repairing the blood-brain barrier. These and other hypothesized reparative roles for fibronectin and laminin after traumatic brain injury are discussed.

Original languageEnglish (US)
Pages (from-to)226-230
Number of pages5
JournalJournal of Neurotrauma
Volume24
Issue number1
DOIs
StatePublished - Jan 1 2007

Fingerprint

Laminin
Fibronectins
Wounds and Injuries
Brain
Regeneration
Extracellular Matrix Proteins
Microglia
Blood-Brain Barrier
Craniocerebral Trauma
Astrocytes
Brain Injuries
Proteins
Cell Death
Animal Models
Macrophages

Keywords

  • Controlled cortical impact
  • Fibronectin
  • Laminin
  • Mouse
  • Traumatic brain injury

ASJC Scopus subject areas

  • Clinical Neurology

Cite this

@article{0a14c098ae2a4aeebd46d64cd836ea57,
title = "Fibronectin and laminin increase in the mouse brain after controlled cortical impact injury",
abstract = "The complex environment of the traumatically injured brain exhibits aspects of inhibition and ongoing cell death together with attempts at repair and regeneration. Elucidating these events and exploiting those factors involved in endogenous repair and regeneration may aid in developing more effective treatments for traumatic brain injury. Two extracellular matrix proteins critical to neural development - fibronectin and laminin - may also play a protective or reparative role in the injury response. While both of these proteins have been found to increase following human brain injury, the presence of these proteins has not been studied in a clinically-relevant animal model of blunt head trauma. In this study, we examined the spatiotemporal profile of both fibronectin and laminin in the mouse brain following controlled cortical impact injury. Fibronectin and laminin reactivity was localized to the injury penumbra up to 14 days post-injury and was significantly higher than uninjured controls at 3 days post-injury. Upon examining the spatial relationship of fibronectin and laminin to support cells, we found macrophages/activated microglia prominently present in the fibronectin-rich tissue, consistent with a role for fibronectin in facilitating debris clearing. Furthermore, reactive astrocyte processes were found sheathing laminin positive vasculature, suggesting that laminin may play a role in repairing the blood-brain barrier. These and other hypothesized reparative roles for fibronectin and laminin after traumatic brain injury are discussed.",
keywords = "Controlled cortical impact, Fibronectin, Laminin, Mouse, Traumatic brain injury",
author = "Tate, {Ciara C.} and Tate, {Matthew C.} and LaPlaca, {Michelle C.}",
year = "2007",
month = "1",
day = "1",
doi = "10.1089/neu.2006.0043",
language = "English (US)",
volume = "24",
pages = "226--230",
journal = "Journal of Neurotrauma",
issn = "0897-7151",
publisher = "Mary Ann Liebert Inc.",
number = "1",

}

Fibronectin and laminin increase in the mouse brain after controlled cortical impact injury. / Tate, Ciara C.; Tate, Matthew C.; LaPlaca, Michelle C.

In: Journal of Neurotrauma, Vol. 24, No. 1, 01.01.2007, p. 226-230.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Fibronectin and laminin increase in the mouse brain after controlled cortical impact injury

AU - Tate, Ciara C.

AU - Tate, Matthew C.

AU - LaPlaca, Michelle C.

PY - 2007/1/1

Y1 - 2007/1/1

N2 - The complex environment of the traumatically injured brain exhibits aspects of inhibition and ongoing cell death together with attempts at repair and regeneration. Elucidating these events and exploiting those factors involved in endogenous repair and regeneration may aid in developing more effective treatments for traumatic brain injury. Two extracellular matrix proteins critical to neural development - fibronectin and laminin - may also play a protective or reparative role in the injury response. While both of these proteins have been found to increase following human brain injury, the presence of these proteins has not been studied in a clinically-relevant animal model of blunt head trauma. In this study, we examined the spatiotemporal profile of both fibronectin and laminin in the mouse brain following controlled cortical impact injury. Fibronectin and laminin reactivity was localized to the injury penumbra up to 14 days post-injury and was significantly higher than uninjured controls at 3 days post-injury. Upon examining the spatial relationship of fibronectin and laminin to support cells, we found macrophages/activated microglia prominently present in the fibronectin-rich tissue, consistent with a role for fibronectin in facilitating debris clearing. Furthermore, reactive astrocyte processes were found sheathing laminin positive vasculature, suggesting that laminin may play a role in repairing the blood-brain barrier. These and other hypothesized reparative roles for fibronectin and laminin after traumatic brain injury are discussed.

AB - The complex environment of the traumatically injured brain exhibits aspects of inhibition and ongoing cell death together with attempts at repair and regeneration. Elucidating these events and exploiting those factors involved in endogenous repair and regeneration may aid in developing more effective treatments for traumatic brain injury. Two extracellular matrix proteins critical to neural development - fibronectin and laminin - may also play a protective or reparative role in the injury response. While both of these proteins have been found to increase following human brain injury, the presence of these proteins has not been studied in a clinically-relevant animal model of blunt head trauma. In this study, we examined the spatiotemporal profile of both fibronectin and laminin in the mouse brain following controlled cortical impact injury. Fibronectin and laminin reactivity was localized to the injury penumbra up to 14 days post-injury and was significantly higher than uninjured controls at 3 days post-injury. Upon examining the spatial relationship of fibronectin and laminin to support cells, we found macrophages/activated microglia prominently present in the fibronectin-rich tissue, consistent with a role for fibronectin in facilitating debris clearing. Furthermore, reactive astrocyte processes were found sheathing laminin positive vasculature, suggesting that laminin may play a role in repairing the blood-brain barrier. These and other hypothesized reparative roles for fibronectin and laminin after traumatic brain injury are discussed.

KW - Controlled cortical impact

KW - Fibronectin

KW - Laminin

KW - Mouse

KW - Traumatic brain injury

UR - http://www.scopus.com/inward/record.url?scp=33846830067&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=33846830067&partnerID=8YFLogxK

U2 - 10.1089/neu.2006.0043

DO - 10.1089/neu.2006.0043

M3 - Article

VL - 24

SP - 226

EP - 230

JO - Journal of Neurotrauma

JF - Journal of Neurotrauma

SN - 0897-7151

IS - 1

ER -