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  • Karward 2019

    Rights statement: This is the author’s version of a work that was accepted for publication in Biochemical Pharmacology. Changes resulting from the publishing process, such as peer review, editing, corrections, structural formatting, and other quality control mechanisms may not be reflected in this document. Changes may have been made to this work since it was submitted for publication. A definitive version was subsequently published in Biochemical Pharmacology, 168, 2019 DOI: 10.1016/j.bcp.2019.07.017

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Endocannabinoids and endocannabinoid-like compounds modulate hypoxia-induced permeability in CaCo-2 cells via CB1, TRPV1, and PPAR<alpha>

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Endocannabinoids and endocannabinoid-like compounds modulate hypoxia-induced permeability in CaCo-2 cells via CB1, TRPV1, and PPAR<alpha> / Karwad, M.A.; Couch, D.G.; Wright, Karen et al.
In: Biochemical Pharmacology, Vol. 168, 01.10.2019, p. 465-472.

Research output: Contribution to Journal/MagazineJournal articlepeer-review

Harvard

Karwad, MA, Couch, DG, Wright, K, Tufarelli, C, Larvin, M, Lund, J & O'Sullivan, SE 2019, 'Endocannabinoids and endocannabinoid-like compounds modulate hypoxia-induced permeability in CaCo-2 cells via CB1, TRPV1, and PPAR<alpha>', Biochemical Pharmacology, vol. 168, pp. 465-472. https://doi.org/10.1016/j.bcp.2019.07.017

APA

Karwad, M. A., Couch, D. G., Wright, K., Tufarelli, C., Larvin, M., Lund, J., & O'Sullivan, S. E. (2019). Endocannabinoids and endocannabinoid-like compounds modulate hypoxia-induced permeability in CaCo-2 cells via CB1, TRPV1, and PPAR<alpha> Biochemical Pharmacology, 168, 465-472. https://doi.org/10.1016/j.bcp.2019.07.017

Vancouver

Karwad MA, Couch DG, Wright K, Tufarelli C, Larvin M, Lund J et al. Endocannabinoids and endocannabinoid-like compounds modulate hypoxia-induced permeability in CaCo-2 cells via CB1, TRPV1, and PPAR<alpha> Biochemical Pharmacology. 2019 Oct 1;168:465-472. Epub 2019 Jul 17. doi: 10.1016/j.bcp.2019.07.017

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Bibtex

@article{c646efa4b9c445228cf01d1f67b1ef78,
title = "Endocannabinoids and endocannabinoid-like compounds modulate hypoxia-induced permeability in CaCo-2 cells via CB1, TRPV1, and PPAR",
abstract = "Background and purposeWe have previously reported that endocannabinoids modulate permeability in Caco-2 cells under inflammatory conditions and hypothesised in the present study that endocannabinoids could also modulate permeability in ischemia/reperfusion.Experimental approachCaco-2 cells were grown on cell culture inserts to confluence. Trans-epithelial electrical resistance (TEER) was used to measure permeability. To generate hypoxia (0% O2), a GasPak{\texttrademark} EZ anaerobe pouch system was used. Endocannabinoids were applied to the apical or basolateral membrane in the presence or absence of receptor antagonists.Key resultsComplete ypoxia decreased TEER (increased permeability) by ∼35% after 4 h (recoverable) and ∼50% after 6 h (non-recoverable). When applied either pre- or post-hypoxia, apical application of N-arachidonoyl-dopamine (NADA, via TRPV1), oleamide (OA, via TRPV1) and oleoylethanolamine (OEA, via TRPV1) inhibited the increase in permeability. Apical administration of anandamide (AEA) and 2-arachidonoylglycerol (2-AG) worsened the permeability effect of hypoxia (both via CB1). Basolateral application of NADA (via TRPV1), OA (via CB1 and TRPV1), noladin ether (NE, via PPARα), and palmitoylethanolamine (PEA, via PPARα) restored permeability after 4 h hypoxia, whereas OEA increased permeability (via PPARα). After 6 h hypoxia, where permeability does not recover, only basolateral application PEA sustainably decreased permeability, and NE decreased permeability.Conclusions and ImplicationsA variety of endocannabinoids and endocannabinoid-like compounds modulate Caco-2 permeability in hypoxia/reoxygenation, which involves multiple targets, depending on whether the compounds are applied to the basolateral or apical membrane. CB1 antagonism and TRPV1 or PPARα agonism may represent novel therapeutic targets against several intestinal disorders associated with increased permeability.",
author = "M.A. Karwad and D.G. Couch and Karen Wright and C. Tufarelli and M. Larvin and J. Lund and S.E. O'Sullivan",
note = "This is the author{\textquoteright}s version of a work that was accepted for publication in Biochemical Pharmacology. Changes resulting from the publishing process, such as peer review, editing, corrections, structural formatting, and other quality control mechanisms may not be reflected in this document. Changes may have been made to this work since it was submitted for publication. A definitive version was subsequently published in Biochemical Pharmacology, 168, 2019 DOI: 10.1016/j.bcp.2019.07.017",
year = "2019",
month = oct,
day = "1",
doi = "10.1016/j.bcp.2019.07.017",
language = "English",
volume = "168",
pages = "465--472",
journal = "Biochemical Pharmacology",
issn = "0006-2952",
publisher = "Elsevier Inc.",

}

RIS

TY - JOUR

T1 - Endocannabinoids and endocannabinoid-like compounds modulate hypoxia-induced permeability in CaCo-2 cells via CB1, TRPV1, and PPAR

AU - Karwad, M.A.

AU - Couch, D.G.

AU - Wright, Karen

AU - Tufarelli, C.

AU - Larvin, M.

AU - Lund, J.

AU - O'Sullivan, S.E.

N1 - This is the author’s version of a work that was accepted for publication in Biochemical Pharmacology. Changes resulting from the publishing process, such as peer review, editing, corrections, structural formatting, and other quality control mechanisms may not be reflected in this document. Changes may have been made to this work since it was submitted for publication. A definitive version was subsequently published in Biochemical Pharmacology, 168, 2019 DOI: 10.1016/j.bcp.2019.07.017

PY - 2019/10/1

Y1 - 2019/10/1

N2 - Background and purposeWe have previously reported that endocannabinoids modulate permeability in Caco-2 cells under inflammatory conditions and hypothesised in the present study that endocannabinoids could also modulate permeability in ischemia/reperfusion.Experimental approachCaco-2 cells were grown on cell culture inserts to confluence. Trans-epithelial electrical resistance (TEER) was used to measure permeability. To generate hypoxia (0% O2), a GasPak™ EZ anaerobe pouch system was used. Endocannabinoids were applied to the apical or basolateral membrane in the presence or absence of receptor antagonists.Key resultsComplete ypoxia decreased TEER (increased permeability) by ∼35% after 4 h (recoverable) and ∼50% after 6 h (non-recoverable). When applied either pre- or post-hypoxia, apical application of N-arachidonoyl-dopamine (NADA, via TRPV1), oleamide (OA, via TRPV1) and oleoylethanolamine (OEA, via TRPV1) inhibited the increase in permeability. Apical administration of anandamide (AEA) and 2-arachidonoylglycerol (2-AG) worsened the permeability effect of hypoxia (both via CB1). Basolateral application of NADA (via TRPV1), OA (via CB1 and TRPV1), noladin ether (NE, via PPARα), and palmitoylethanolamine (PEA, via PPARα) restored permeability after 4 h hypoxia, whereas OEA increased permeability (via PPARα). After 6 h hypoxia, where permeability does not recover, only basolateral application PEA sustainably decreased permeability, and NE decreased permeability.Conclusions and ImplicationsA variety of endocannabinoids and endocannabinoid-like compounds modulate Caco-2 permeability in hypoxia/reoxygenation, which involves multiple targets, depending on whether the compounds are applied to the basolateral or apical membrane. CB1 antagonism and TRPV1 or PPARα agonism may represent novel therapeutic targets against several intestinal disorders associated with increased permeability.

AB - Background and purposeWe have previously reported that endocannabinoids modulate permeability in Caco-2 cells under inflammatory conditions and hypothesised in the present study that endocannabinoids could also modulate permeability in ischemia/reperfusion.Experimental approachCaco-2 cells were grown on cell culture inserts to confluence. Trans-epithelial electrical resistance (TEER) was used to measure permeability. To generate hypoxia (0% O2), a GasPak™ EZ anaerobe pouch system was used. Endocannabinoids were applied to the apical or basolateral membrane in the presence or absence of receptor antagonists.Key resultsComplete ypoxia decreased TEER (increased permeability) by ∼35% after 4 h (recoverable) and ∼50% after 6 h (non-recoverable). When applied either pre- or post-hypoxia, apical application of N-arachidonoyl-dopamine (NADA, via TRPV1), oleamide (OA, via TRPV1) and oleoylethanolamine (OEA, via TRPV1) inhibited the increase in permeability. Apical administration of anandamide (AEA) and 2-arachidonoylglycerol (2-AG) worsened the permeability effect of hypoxia (both via CB1). Basolateral application of NADA (via TRPV1), OA (via CB1 and TRPV1), noladin ether (NE, via PPARα), and palmitoylethanolamine (PEA, via PPARα) restored permeability after 4 h hypoxia, whereas OEA increased permeability (via PPARα). After 6 h hypoxia, where permeability does not recover, only basolateral application PEA sustainably decreased permeability, and NE decreased permeability.Conclusions and ImplicationsA variety of endocannabinoids and endocannabinoid-like compounds modulate Caco-2 permeability in hypoxia/reoxygenation, which involves multiple targets, depending on whether the compounds are applied to the basolateral or apical membrane. CB1 antagonism and TRPV1 or PPARα agonism may represent novel therapeutic targets against several intestinal disorders associated with increased permeability.

U2 - 10.1016/j.bcp.2019.07.017

DO - 10.1016/j.bcp.2019.07.017

M3 - Journal article

VL - 168

SP - 465

EP - 472

JO - Biochemical Pharmacology

JF - Biochemical Pharmacology

SN - 0006-2952

ER -