CoChat
Sign Up
Cited by 254Barrier Structure and Function StudiesChemokine receptors and signalingAcute Ischemic Stroke Management

The DOI matches its Crossref record; 54 of the 55 references it cites were found in a registry or an index.

Effects of the Chemokine CCL2 on Blood–Brain Barrier Permeability during Ischemia–Reperfusion Injury

Dimitrijevic, Oliver B, Stamatovic, Svetlana M, Keep, Richard F, Andjelkovic, Anuska V·2006·Journal of Cerebral Blood Flow & Metabolism
DOI 10.1038/sj.jcbfm.9600229
Open this paper in CoChat — free account

Abstract

The chemokine CCL2 is considered as one of the main effectors driving postischemic infiltration of monocytes into the brain parenchyma. New experimental data, however, suggest that CCL2 could also participate in blood–brain barrier (BBB) ‘opening’ during the transmigration of monocytes. The current study examines the role of CCL2 in regulating BBB permeability after ischemia in vitro. To address this issue, an in vitro BBB model (coculture of astrocytes and brain endothelial cells) was subjected to 5 h of oxygen glucose deprivation, followed by reoxgenation ( in vitro ischemia/reperfusion (I/R)) for 0 to 48 h. During reperfusion, there was a biphasic enhancement of barrier permeability, with a 200-fold increase in barrier permeability to FITC-albumin at 6 h and a further period of disruption around 24 h. The latter coincided with increased secretion of CCL2 by both astrocytes and brain endothelial cells and increased levels of the CCL2 receptor, CCR2. Applying antisense oligonucleotide or neutralizing antibody to block CCL2 significantly decreased I/R-induced enhancement of BBB permeability (approximately twofold) and redistribution of tight-junction (TJ) proteins (occludin, zonula occluden-1, 2, claudin-5). Similarly, absence of CCR2 from endothelial cells caused stabilization of TJ complexes and decreased the permeability of brain endothelial barrier during in vitro I/R. These data suggest CCL2/CCR2 has an important role in regulating brain endothelial permeability and might be a potential novel therapeutic target for stroke.

Overview

Integrity signals

Registry

Crossref · 10.1038/sj.jcbfm.9600229

Cites

54 of 54 references verified0 citation errors · 0 not checkable

Statistics

Recomputing p-values needs the paper’s full text.

Verification

Claims the paper makes

This paper’s full text isn’t openly available, so its claims and self-check weren’t run. The registry and citation checks still apply.

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

Citations

Cites

Show all 55 references

Research works printed but not linked: 10

  1. Abbruscato TJ, 1999, J Pharmacol Exp Ther, 289, 668
  2. Couraud PO, 1998, Pathol Biol (Paris), 46, 176
  3. Dirnagl U, 1999, TINS, 22, 391
  4. Huber JD, 2001, TINS, 24, 719
  5. Matsumoto T, 1997, Lab Invest, 77, 119
  6. Menicken F, 1999, TIPS, 20, 73
  7. Nakagawa Y, 1990, Adv Neurol, 52, 21
  8. 10.1182/blood.V90.3.909 · DOI
  9. Schuerer L, 1994, Acta Neurochir Suppl, 60, 51
  10. Stoll G, 2002, Adv Exp Med Biol, 513, 87

Cited by

Sorted by citations

See all 254

Related

Metadata

Authors
Dimitrijevic, O. B., Stamatovic, S. M., Keep, R. F., & Andjelkovic, A. V.
Affiliations
University of Michigan (US)
Corresponding author
Andjelkovic, Anuska V
ORCID
Venue
Journal of Cerebral Blood Flow & Metabolism
Publisher
SAGE Publications
Published
2006-06
Volume
26
Issue
6
Pages
797-810
ISSN
  • 0271-678X (ISSN-L)
  • 1559-7016
DOI
10.1038/sj.jcbfm.9600229
OpenAlex
W1995446848
Cited by
252
References
55
Citations by year
2026: 7 · 2025: 11 · 2024: 26 · 2023: 18 · 2022: 19 · 2021: 10 · 2020: 12 · 2019: 9 · 2018: 16 · 2017: 13 · 2016: 11 · 2015: 9 · 2014: 16 · 2013: 16 · 2012: 11
FWCI
2.62
Type
journal article
Language
en
Open access
closed
Licence
journals.sagepub.com/page/policies/text-and-data-mining-license (tdm)
Locations
  • Journal of Cerebral Blood Flow & Metabolism (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • University of Michigan
  • National Institute of Neurological Disorders and Stroke (R01NS044907, NS-044907)
  • Division of Chemistry
Topics
  • Life Sciences › Neuroscience › Neurology › Barrier Structure and Function Studies
  • Health Sciences › Medicine › Oncology › Chemokine receptors and signaling
  • Health Sciences › Medicine › Clinical Neurology › Acute Ischemic Stroke Management
Keywords
MCP-1, CCR2, blood-brain barrier permeability, ischemia-reperfusion injury, monocyte transmigration, tight junction proteins, occludin, claudin-5, zonula occludens-1, brain endothelial cells, astrocytes, oxygen-glucose deprivation, stroke, chemokines
MeSH terms
Animals, Astrocytes, Blood-Brain Barrier, Capillary Permeability, Cell Movement, Cells, Cultured, Enzyme-Linked Immunosorbent Assay, Fluorescent Antibody Technique, Blotting, Western, Reperfusion Injury, Electric Impedance, Coculture Techniques, Chemokine CCL2, Receptors, Chemokine, Reverse Transcriptase Polymerase Chain Reaction, Endothelial Cells, Mice, Receptors, CCR2

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review