Evidence map›Paper›PMID 11717355›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2001

The chemokine receptor CCR2 mediates the binding and internalization of monocyte chemoattractant protein-1 along brain microvessels.

K A Dzenko, A V Andjelkovic, W A Kuziel, J S Pachter

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.7field-weighted citation impact, top 10% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

30 citing papers in PubMed, 89 citations in OpenAlex.

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  13. CCR2 antagonism alters brain macrophage polarization and ameliorates cognitive dysfunction induced by traumatic brain injury.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015
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  16. CCR2+ Ly6C(hi) inflammatory monocyte recruitment exacerbates acute disability following intracerebral hemorrhage.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014
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  19. CCL2 disrupts the adherens junction: implications for neuroinflammation.Laboratory investigation; a journal of technical methods and pathology · 2012
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 2 institutions in 1 country.

K A DzenkoBlood-Brain Barrier Laboratory, Department of Pharmacology, University of Connecticut Health Center, Farmington, Connecticut 06030, USA.
A V Andjelkovic
W A Kuziel
J S Pachter
UConn Health · USThe University of Texas at Austin · US

Funding

CNS INFLAMMATION IN NERVOUS AND MENTAL DISEASER01MH054718 · NIMH · UNIVERSITY OF CONNECTICUT SCH OF MED/DNT · PI PACHTER, JOEL S · 1996 to 2005
$1.2M
NIMH NIH HHS 1RO1-MH54718-01A1NIMH NIH HHS R01 MH054718
6 · The paper itself

Abstract

Previous results from this laboratory revealed the presence of high-affinity saturable binding sites for monocyte chemoattractant protein-1 (MCP-1) along human brain microvessels (Andjelkovic et al., 1999; Andjelkovic and Pachter, 2000), which suggested that CC chemokine receptor 2 (CCR2), the recognized receptor for this chemokine, was expressed by the brain microvascular endothelium. To test the role of CCR2 directly in mediating MCP-1 interactions with the brain microvasculature, we assessed MCP-1 binding activity in murine brain microvessels isolated from wild-type mice and from CCR2 (-/-) mice engineered to lack this receptor. Results demonstrate that MCP-1 binding is greatly attenuated in microvessels prepared from CCR2 (-/-) mice compared with wild-type controls. Moreover, microvessels from wild-type mice exhibited MCP-1-induced downmodulation in MCP-1 binding and a recovery of binding activity that was not dependent on de novo protein synthesis. Furthermore, MCP-1 was shown to be internalized within wild-type microvessels, but not within microvessels obtained from CCR2 (-/-) mice, additionally demonstrating that CCR2 is obligatory for MCP-1 endocytosis. Last, internalization of MCP-1, but not transferrin, was observed to be inhibited by disruption of caveolae. Internalized MCP-1 also colocalized at some sites with caveolin-1, a major protein of caveolae, implying that this chemokine is endocytosed, in part, via nonclathrin-coated vesicles. These results prompt consideration that MCP-1 signals may be relayed across the blood-brain barrier by highly specialized interactions of this chemokine with its cognate receptor, CCR2, along brain microvascular endothelial cells.

Indexed as

AnimalsBinding, CompetitiveBrainCaveolaeCaveolin 1CaveolinsChemokine CCL2ChemokinesCrosses, GeneticDown-RegulationEndocytosisEndothelium, VascularFilipinIn Vitro TechniquesLigandsMiceCav1 protein, mouseCaveolin 1CaveolinsCCR2 protein, humanCcr2 protein, mouseChemokine CCL2ChemokinesFilipinLigandsReceptors, CCR2Receptors, ChemokineTransferrin

Identifiers

PMID11717355
PMCPMC6763923
OpenAlexW1516141774

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.