Human mast cells take up and hydrolyze anandamide under the control of 5‐lipoxygenase and do not express cannabinoid receptors

Maccarrone, Mauro; Fiorucci, Laura; Erba, Fulvio; Bari, Monica; Finazzi‐Agrò, Alessandro; Ascoli, Franca

doi:10.1016/s0014-5793(00)01223-0

Cited by 87 publications

(79 citation statements)

References 34 publications

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“…The K M values estimated for the facilitated transport component of AEA are rather similar to those found previously (Hillard et al, 1997;Bisogno et al, 1997;Rakhshan et al, 2000), although other authors have reported K M values near or below 1 mM Maccarrone et al, 1998;2000b). One explanation for this discrepancy may be di erences in curve ®tting techniques (see Rakhshan et al, 2000), and it can be noted that in a recent study using human CCF-STTG1 astrocytoma cells, the IC 50 of non-radioactive AEA as an inhibitor of the uptake of 30 nM AEA (15.1+3.0 mM) was considerably higher than its K M value (0.6+0.1 mM) .…”

Section: Discussionsupporting

confidence: 89%

Characterization of palmitoylethanolamide transport in mouse Neuro‐2a neuroblastoma and rat RBL‐2H3 basophilic leukaemia cells: comparison with anandamide

Jacobsson

Fowler

2001

British J Pharmacology

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1 The endogenous cannabinoid receptor agonist anandamide (AEA) and the related compound palmitoylethanolamide (PEA) are inactivated by transport into cells followed by metabolism by fatty acid amide hydrolase (FAAH). The cellular uptake of AEA has been characterized in detail, whereas less is known about the properties of the PEA uptake, in particular in neuronal cells. In the present study, the pharmacological and functional properties of PEA and AEA uptake have been investigated in mouse Neuro-2a neuroblastoma and, for comparison, in rat RBL-2H3 basophilic leukaemia cells. 2 Saturable uptake of PEA and AEA into both cell lines were demonstrated with apparent K M values of 28 mM (PEA) and 10 mM (AEA) in Neuro-2a cells, and 30 mM (PEA) and 9.3 mM (AEA) in RBL-2H3 cells. Both PEA and AEA uptake showed temperature-dependence but only the AEA uptake was sensitive to treatment with Pronase and phenylmethylsulfonyl¯uoride. 3 The AEA uptake was inhibited by AM404, 2-arachidonoylglycerol (2-AG), R1-and S1-methanandamide, arachidonic acid and olvanil with similar potencies for the two cell types. PEA, up to a concentration of 100 mM, did not a ect AEA uptake in either cell line. AEA, 2-AG, arachidonic acid, R1-methanandamide, D 9 -THC, and cannabidiol inhibited PEA transport in both cell lines. The non-steroidal anti-in¯ammatory drug indomethacin inhibited the AEA uptake but had very weak e ects on the uptake of PEA. 4 From these data, it can be concluded that PEA is transported in to cells both by passive di usion and by a facilitated transport that is pharmacologically distinguishable from AEA uptake.

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Section: Discussionsupporting

confidence: 89%

Characterization of palmitoylethanolamide transport in mouse Neuro‐2a neuroblastoma and rat RBL‐2H3 basophilic leukaemia cells: comparison with anandamide

Jacobsson

Fowler

2001

British J Pharmacology

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“…However, no expression of these two receptors was detected in HMC-1 cells [42]. Thus, in line with the hypothesis that some effects of endocannabinoids are mediated by the GPR55 receptor [22], either GPR55 mRNA and protein were detected in HMC-1 cells.…”

supporting

confidence: 66%

Endocannabinoids inhibit release of nerve growth factor by inflammation-activated mast cells

Cantarella

Scollo

Lempereur

et al. 2011

Biochemical Pharmacology

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“…FABPs may also provide a means for rapid substrate delivery to other enzymes with distinct subcellular localizations capable of metabolizing AEA to a minor degree (34,52,53). Relative to other AEA uptake models, the proposed mechanism of simple diffusion across the plasma membrane and subsequent cytosolic trafficking by FABPs provides the most temporally efficient mode of AEA delivery to FAAH.…”

Section: Discussionmentioning

confidence: 99%

Identification of intracellular carriers for the endocannabinoid anandamide

Kaczocha¹,

Glaser

Deutsch³

2009

Proc. Natl. Acad. Sci. U.S.A.

308

332

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The endocannabinoid anandamide (arachidonoyl ethanolamide, AEA) is an uncharged neuromodulatory lipid that, similar to many neurotransmitters, is inactivated through its cellular uptake and subsequent catabolism. AEA is hydrolyzed by fatty acid amide hydrolase (FAAH), an enzyme localized on the endoplasmic reticulum. In contrast to most neuromodulators, the hydrophilic cytosol poses a diffusional barrier for the efficient delivery of AEA to its site of catabolism. Therefore, AEA likely traverses the cytosol with the assistance of an intracellular carrier that increases its solubility and rate of diffusion. To study this process, AEA uptake and hydrolysis were examined in COS-7 cells expressing FAAH restricted to the endoplasmic reticulum, mitochondria, or the Golgi apparatus. AEA hydrolysis was detectable at the earliest measurable time point (

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Human mast cells take up and hydrolyze anandamide under the control of 5‐lipoxygenase and do not express cannabinoid receptors

Cited by 87 publications

References 34 publications

Characterization of palmitoylethanolamide transport in mouse Neuro‐2a neuroblastoma and rat RBL‐2H3 basophilic leukaemia cells: comparison with anandamide

Characterization of palmitoylethanolamide transport in mouse Neuro‐2a neuroblastoma and rat RBL‐2H3 basophilic leukaemia cells: comparison with anandamide

Endocannabinoids inhibit release of nerve growth factor by inflammation-activated mast cells

Identification of intracellular carriers for the endocannabinoid anandamide

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