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Cited by 56Barrier Structure and Function StudiesIon Channels and ReceptorsIon Transport and Channel Regulation

Regulation of blood-brain barrier permeability by transient receptor potential type C and type v calcium-permeable channels

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Brown, Rachel C., Wu, Ling, Hicks, Kali, O'neil, Roger G.·2008·Microcirculation
DOI 10.1080/10739680701762656PMC PMC3077823
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Abstract

Objective: To identify plasma membrane ion channels mediating calcium influx at the blood‐brain barrier in response to disrupting stimuli. Methods: We examined the expression and function of candidate transient receptor potential channels using reverse transcriptase polymerase chain recation, Fura‐2 calcium imaging, and permeability assays. Results: Immortalized mouse brain microvessel endothelial cells expressed multiple transient receptor potential isoforms: transient receptor potential C1, C2, C4, and C7, M2, M3, M4, and M7, and V2 and V4. Similar profiles were observed in freshly isolated cerebral microvessels and primary cultured rat brain endothelial cells. Thrombin‐stimulated calcium influx in brain endothelial cells was blocked by transient receptor potential C inhibitors. Transient receptor potential V activating stimuli also increased intracellular calcium. This increase was inhibited by a transient receptor potential V blocker or by removal of extracellular calcium. Barrier integrity was compromised by thrombin, hypo‐osmolar stress, and PMA treatment. The increase in barrier permeability induced by transient receptor potential V activators was blocked by transient receptor potential V inhibition, while thrombin effects were inhibited by transient receptor potential C inhibitors. Conclusions: These results demonstrate that transient receptor potential C and transient receptor potential V channels mediate calcium influx at the blood‐brain barrier, and as a consequence, may modulate barrier integrity.

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  • Activation of SGK1 can increase cytoplasmic calcium levels, thereby compromising integrity of BBB.

    “activation of SGK1, which can increase cytoplasmic calcium levels, thereby compromising the integrity of the BBB”

    From Serum/glucocorticoid regulated kinase 1 (SGK1) in neurological disorders: pain or gain (2024) · cites this paper as Brown et al., 2008

    The Conclusions (page unavailable) say that TRPC and TRPV channels mediate calcium influx at the BBB and may modulate barrier integrity. The Discussion (page unavailable) also links increased intracellular calcium and altered barrier permeability. Our copy does not identify SGK1 as the activator or establish that activating it compromises the BBB; searches for SGK1 and serum glucocorticoid-regulated kinase found no supporting passage. (LLM, conf=0.86)

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Cited by

Sorted by citations

Authors
Brown, R. C., Wu, L., Hicks, K., & O'neil, R. G.
Affiliations
The University of Texas Health Science Center at Houston (US)
ORCID
Wu, Ling
Venue
Microcirculation
Publisher
Wiley
Published
2008-05
Volume
15
Issue
4
Pages
359-371
ISSN
  • 1073-9688 (ISSN-L)
  • 1549-8719
DOI
10.1080/10739680701762656
PMC
PMC3077823
OpenAlex
W2084717111
Cited by
56
References
0
Citations by year
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FWCI
1.32
Type
journal article
Language
en
Open access
Licence
onlinelibrary.wiley.com/termsAndConditions#vor (vor, 635 d)
Locations
  • Microcirculation (publishedVersion)
  • PubMed (publishedVersion)
  • Europe PMC (PubMed Central) (acceptedVersion)
  • PubMed Central (acceptedVersion)
Funders
National Institute of Diabetes and Digestive and Kidney Diseases (R01DK070950)
Topics
  • Life Sciences › Neuroscience › Neurology › Barrier Structure and Function Studies
  • Life Sciences › Neuroscience › Sensory Systems › Ion Channels and Receptors
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ion Transport and Channel Regulation
Keywords
blood-brain barrier permeability, TRP channels, TRPC channels, TRPV channels, calcium influx, brain endothelial cells, thrombin, hypoosmotic stress, phosphatidylcholine, barrier integrity, calcium-permeable channels
MeSH terms
Animals, Blood-Brain Barrier, Calcium, Calcium Channel Blockers, Cell Line, Osmotic Pressure, Permeability, Thrombin, Endothelial Cells, TRPC Cation Channels, TRPV Cation Channels, Mice

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