Language:

The Acute-Phase Protein PTX3 is an Essential Mediator of Glial Scar Formation and Resolution of Brain Edema after Ischemic Injury

Journal of cerebral blood flow and metabolism, 2014-03, Vol.34 (3), p.480-488 [Peer Reviewed Journal]

2014 ISCBFM ;Copyright © 2014 International Society for Cerebral Blood Flow & Metabolism, Inc. 2014 International Society for Cerebral Blood Flow & Metabolism, Inc. ;ISSN: 0271-678X ;EISSN: 1559-7016 ;DOI: 10.1038/jcbfm.2013.224 ;PMID: 24346689

Full text available

Citations Cited by

Actions
1. Add to My Research
2. Remove from My Research
3. E-mail
4. Print
5. Permalink
6. Citation
7. EasyBib
8. EndNote
9. RefWorks
10. Delicious
11. Export RIS
12. Export BibTeX

Title:
The Acute-Phase Protein PTX3 is an Essential Mediator of Glial Scar Formation and Resolution of Brain Edema after Ischemic Injury
Author: Rodriguez-Grande, Beatriz ; Swana, Matimba ; Nguyen, Loan ; Englezou, Pavlos ; Maysami, Samaneh ; Allan, Stuart M ; Rothwell, Nancy J ; Garlanda, Cecilia ; Denes, Adam ; Pinteaux, Emmanuel
Subjects: Animals ; Brain Edema - etiology ; Brain Edema - immunology ; Brain Edema - metabolism ; Brain Edema - pathology ; Brain Ischemia - complications ; Brain Ischemia - immunology ; Brain Ischemia - metabolism ; Brain Ischemia - pathology ; C-Reactive Protein - genetics ; C-Reactive Protein - metabolism ; Cell Proliferation - drug effects ; Cicatrix - immunology ; Cicatrix - metabolism ; Cicatrix - pathology ; Disease Models, Animal ; Enzyme-Linked Immunosorbent Assay ; Gene Expression - drug effects ; Interleukin-1alpha - genetics ; Interleukin-1alpha - immunology ; Interleukin-1alpha - pharmacology ; Interleukin-1beta - genetics ; Interleukin-1beta - immunology ; Interleukin-1beta - pharmacology ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Nerve Tissue Proteins - genetics ; Nerve Tissue Proteins - metabolism ; Neuroglia - immunology ; Neuroglia - metabolism ; Neuroglia - pathology ; Original
Is Part Of: Journal of cerebral blood flow and metabolism, 2014-03, Vol.34 (3), p.480-488
Description: Acute-phase proteins (APPs) are key effectors of the immune response and are routinely used as biomarkers in cerebrovascular diseases, but their role during brain inflammation remains largely unknown. Elevated circulating levels of the acute-phase protein pentraxin-3 (PTX3) are associated with worse outcome in stroke patients. Here we show that PTX3 is expressed in neurons and glia in response to cerebral ischemia, and that the proinflammatory cytokine interleukin-1 (IL-1) is a key driver of PTX3 expression in the brain after experimental stroke. Gene deletion of PTX3 had no significant effects on acute ischemic brain injury. In contrast, the absence of PTX3 strongly compromised blood–brain barrier integrity and resolution of brain edema during recovery after ischemic injury. Compromised resolution of brain edema in PTX3-deficient mice was associated with impaired glial scar formation and alterations in scar-associated extracellular matrix production. Our results suggest that PTX3 expression induced by proinflammatory signals after ischemic brain injury is a critical effector of edema resolution and glial scar formation. This highlights the potential role for inflammatory molecules in brain recovery after injury and identifies APPs, in particular PTX3, as important targets in ischemic stroke and possibly other brain inflammatory disorders.
Publisher: London, England: SAGE Publications
Language: English
Identifier: ISSN: 0271-678X
EISSN: 1559-7016
DOI: 10.1038/jcbfm.2013.224
PMID: 24346689
Source: Freely Accessible Journals
Open Access: PubMed Central
AUTh Library subscriptions: ProQuest Central
MEDLINE

Back to results list


INSPIRE LIBRARY - TON DUC THANG UNIVERSITY	(84-028) 37 755 057	Feedback
19 Nguyen Huu Tho St. Dist.7, HCM	thuvien@tdtu.edu.vn	Feedback

The Acute-Phase Protein PTX3 is an Essential Mediator of Glial Scar Formation and Resolution of Brain Edema after Ischemic Injury

2014 ISCBFM ;Copyright © 2014 International Society for Cerebral Blood Flow & Metabolism, Inc. 2014 International Society for Cerebral Blood Flow & Metabolism, Inc. ;ISSN: 0271-678X ;EISSN: 1559-7016 ;DOI: 10.1038/jcbfm.2013.224 ;PMID: 24346689

Searching Remote Databases, Please Wait