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Anionic linear aliphatic surfactants activate TRPV1: a possible endpoint for estimation of detergent induced eye nociception?
Stockholms universitet, Naturvetenskapliga fakulteten, Institutionen för neurokemi.
Stockholms universitet, Naturvetenskapliga fakulteten, Institutionen för neurokemi.
Stockholms universitet, Naturvetenskapliga fakulteten, Institutionen för neurokemi.
Stockholms universitet, Naturvetenskapliga fakulteten, Institutionen för neurokemi.
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2009 (Engelska)Ingår i: Toxicology in Vitro, ISSN 0887-2333, E-ISSN 1879-3177, Vol. 23, nr 8, s. 1472-1476Artikel i tidskrift (Refereegranskat) Published
Abstract [en]

The transient receptor potential vanilloid type 1 (TRPV1) has been reported as one of the key components in the pain pathway. Activation of the receptor causes a Ca2+ influx in sensory C-fibres with secondary effects leading to neurogenic inflammation in the surrounding tissue. We have earlier reported specific activation of TRPV1 by surfactant-containing hygiene products. We have continued this project by investigating activation of the TRPV1 by shampoo and soap ingredients in low concentrations measured as intracellular Ca2+ influxes in stably TRPV1-expressing neuroblastoma SH-SY5Y cells. As a TRPV1 specific control, the TRPV1 antagonist capsazepine was used. The response was quantified as the product induced Ca2+ influx during 2 min in relation to the maximum response induced by the TRPV1 agonist capsaicin. The results show that anionic alkyl linear surfactant ingredients such as sodium lauryl sulphate, sodium laureth sulphate, ammonium lauryl sulphate, sodium C12-15 pareth sulphate and N-lauroylsarcosine concentration-dependently induced Ca2+ influx that could be addressed to TRPV1. The cationic surfactants benzalkonium chloride and cetylpyridinium chloride induced a Ca2+ influx that was not TRPV1 mediated as well as the zwitterionic surfactant cocamidopropyl betaine, the non-linear anionic surfactant sodium deoxycholate and the non-ionic surfactant Triton-X. These results reveal a new mechanistic pathway for surfactant-induced nociception.

Ort, förlag, år, upplaga, sidor
2009. Vol. 23, nr 8, s. 1472-1476
Identifikatorer
URN: urn:nbn:se:su:diva-32269DOI: 10.1016/j.tiv.2009.06.013ISI: 000272276600006PubMedID: 19540328OAI: oai:DiVA.org:su-32269DiVA, id: diva2:279973
Tillgänglig från: 2009-12-07 Skapad: 2009-12-07 Senast uppdaterad: 2017-12-12Bibliografiskt granskad
Ingår i avhandling
1. Activation and Regulation of TRPV1: Studies in Recombinant Human Neuroblastoma TRPV1-SHSY5Y Cells
Öppna denna publikation i ny flik eller fönster >>Activation and Regulation of TRPV1: Studies in Recombinant Human Neuroblastoma TRPV1-SHSY5Y Cells
2009 (Engelska)Doktorsavhandling, sammanläggning (Övrigt vetenskapligt)
Abstract [en]

TRPV1 is a transmembrane non-selective cation channel with preference for Ca2+. The receptor is primarily localised on dorsal root ganglion neurons and is activated by numerous endogenous and exogenous potentially irritating ligands eliciting pain. The TRPV1 expression and activity are regulated by several neurotrophic agents and inflammatory mediators via activation of phosphorylation cascades.

In this thesis a stably TRPV1-expressing cell clone of the human neuroblastoma cell line SHSY5Y was established with the purpose to study regulation of TRPV1 through a straightforward and reproducible approach.

In paper I it is reported that the neurotrophic factors insulin, and IGF-1 up-regulate TRPV1 in the TRPV1-SHSY5Y cells. Additionally, the involved signalling pathways are suggested. This is of interest because both TRPV1 activity and expression is altered in diabetic patients with painful neuropathies, and so is insulin and IGF-1 signalling.

Results from paper II show that the neuronally differentiating morphogen retinoic acid (RA) increases TRPV1 protein levels and TRPV1-mediated Ca2+ influxes. Furthermore, the basal Ca2+ level is increased after RA treatment in TRPV1-SHSY5Y cells but not in native SHSY5Y cells. The TRPV1-SHSY5Y cells also develop into a more mature neuronal phenotype than the native SHSY5Y cells after six days of RA-induced differentiation. Hence, TRPV1 might be involved in neurogenesis.

In paper III-IV it is concluded that the TRPV1-SHSY5Y cells can be used in a semi-high throughput screening (HTS)-mode to adress TRPV1-mediated Ca2+ influxes. In this assay it is shown that anionic linear aliphatic surfactants might be potent ligands of TRPV1. As a concluding remark, the TRPV1–SHSY5Y cells can be utilised to assess activation and regulation of TRPV1 in an easy-to-use and robust model system.

Ort, förlag, år, upplaga, sidor
Stockholm: Department of Neurochemistry, Stockholm University, 2009. s. 91
Nyckelord
nociception, neurotrophic factors, eye irritation, stable transfection, Ca2+
Nationell ämneskategori
Neurovetenskaper
Forskningsämne
neurokemi med molekylär neurobiologi
Identifikatorer
urn:nbn:se:su:diva-30182 (URN)978-91-7155-954-8 (ISBN)
Disputation
2009-11-13, Magnélisalen, Kemiska övningslaboratoriet, Svante Arrhenius väg 16 B, Stockholm, 13:00 (Engelska)
Opponent
Handledare
Anmärkning
At the time of the doctoral defense, the following papers were unpublished and had a status as follows: Paper 3: In press. Paper 4: In press.Tillgänglig från: 2009-10-22 Skapad: 2009-10-06 Senast uppdaterad: 2018-01-13Bibliografiskt granskad

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