Transcellular transport of CCL2 across brain microvascular endothelial cells
Abstract
The means by which the chemokine CCL2 produced in the brain parenchyma can recruit leukocytes lying behind the highly impervious endothelium of the blood–brain barrier (BBB) has remained a paradox. As other chemokines have been evidenced to stimulate their own synthesis and release by peripheral microvascular endothelial cells, and/or undergo transcytosis in the abluminal‐to‐luminal direction, we determined whether CCL2 experiences similar fates across brain microvascular endothelial cells (BMEC). Using cultured BMEC as a paradigm of the BBB, it was observed that exogenous unlabeled CCL2 actually depressed the release of endogenous CCL2, and further caused diminished CCL2 mRNA levels in these cells. On the other hand, exogenous 125 I‐labeled CCL2 exhibited transport across BMEC in a manner that was sensitive to temperature, competition by excess unlabeled CCL2 but not unlabeled CCL3, knockdown of caveolin‐1/caveolae, and elimination of the cognate CCL2 receptor CCR2. These results implied a facet of CCL2 transport by a transcellular mechanism partly involving binding of CCL2 to CCR2, and subsequent transfer to caveolae vesicles for transcytosis. This notion was supported by double‐label immuno‐electronmicroscopy, which revealed co‐localization of caveolin‐1 with exogenous CCL2, during this chemokine’s transit across BMEC. Collectively, these findings provide a rationale by which CCL2, deposited on the abluminal side of the brain microvasculature during inflammatory episodes, can be relayed across the BBB to foster leukocyte recruitment.
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CCL-2 is predominantly pro-inflammatory.
“This chemokine is predominantly pro-inflammatory and has been implicated in the chemotaxis of peripheral monocytes to the brain [43].”
CCL-2 has been implicated in the chemotaxis of peripheral monocytes to the brain.
“This chemokine is predominantly pro-inflammatory and has been implicated in the chemotaxis of peripheral monocytes to the brain [43].”
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- Authors
- Ge, S., Song, L., Serwanski, D. R., Kuziel, W. A., & Pachter, J. S.
- Affiliations
- UConn Health (US)
- University of Connecticut (US)
- PDL BioPharma (United States) (US)
- ORCID
- Ge, Shujun
- Venue
- Journal of Neurochemistry
- Publisher
- Wiley
- Published
- 2007-10-09
- Volume
- 104
- Issue
- 5
- Pages
- 1219-1232
- ISSN
- 0022-3042 (ISSN-L)
- 1471-4159
- OpenAlex
- W2003365576
- Cited by
- 83
- References
- 79
- Citations by year
- 2026: 1 · 2025: 3 · 2024: 2 · 2023: 6 · 2022: 4 · 2021: 4 · 2020: 3 · 2019: 3 · 2018: 3 · 2017: 3 · 2016: 3 · 2015: 6 · 2014: 8 · 2013: 3 · 2012: 6
- FWCI
- 4.02
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Journal of Neurochemistry (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (RG-2633)
- National Institute of Mental Health (R0-1-MH5478)
- Topics
- Life Sciences › Neuroscience › Neurology › Barrier Structure and Function Studies
- Health Sciences › Medicine › Oncology › Chemokine receptors and signaling
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Caveolin-1 and cellular processes
- Keywords
- MCP-1, blood-brain barrier, brain microvascular endothelial cells, CCR2, caveolin-1, caveolae, leukocyte recruitment, chemokine receptor signaling, neuroinflammation
- MeSH terms
- Animals, Biological Transport, Active, Blood-Brain Barrier, Brain, Capillary Permeability, Cell Membrane, Cells, Cultured, Chemotaxis, Leukocyte, Endothelium, Vascular, Mice, Inbred C57BL, Microcirculation, Mice, Knockout, Chemokine CCL2, Mice
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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 ›
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