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Title: Capsaicin stimulates the non-store-operated Ca{sup 2+} entry but inhibits the store-operated Ca{sup 2+} entry in neutrophils

Abstract

Rat neutrophils express the mRNA encoding for transient receptor potential (TRP) V1. However, capsaicin-stimulated [Ca{sup 2+}]{sub i} elevation occurred only at high concentrations ({>=}100 {mu}M). This response was substantially decreased in a Ca{sup 2+}-free medium. Vanilloids displayed similar patterns of Ca{sup 2+} response with the rank order of potency as follows: scutigeral>resiniferatoxin>capsazepine>capsaicin=olvanil>isovelleral. Arachidonyl dopamine (AAD), an endogenous ligand for TRPV1, failed to desensitize the subsequent capsaicin challenge. Capsaicin-induced Ca{sup 2+} response was not affected by 8-bromo-cyclic ADP-ribose (8-Br-cADPR), the ryanodine receptor blocker, but was slightly attenuated by 1-[6-[17{beta}-3-methoxyestra-1,3,5(10)-trien-17-yl]amino]hexyl]-1H-pyrrole-2,= 5-dione (U-73122), the inhibitor of phospholipase C-coupled processes, 1-[{beta}-[3-(4-methoxyphenyl)propoxy]-4-methoxyphenethyl]-1H-imidazole (SKF-96365), the blocker of receptor-gated and store-operated Ca{sup 2+} (SOC) channels, 2-aminoethyldiphenyl borate (2-APB), the blocker of D-myo-inositol 1,4,5-trisphospahte (IP{sub 3}) receptor and Ca{sup 2+} influx, and by ruthenium red, a blocker of TRPV channels, and enhanced by the Ca{sup 2+} channels blocker, cis-N-(2-phenylcyclopentyl)azacyclotridec-1-en-2-amine (MDL-12330A) and Na{sup +}-deprivation. In addition, capsaicin had no effect on the plasma membrane Ca{sup 2+}-ATPase activity or the production of nitric oxide (NO) and reactive oxygen intermediates (ROI) or on the total thiols content. Capsaicin ({>=}100 {mu}M) inhibited the cyclopiazonic acid (CPA)-induced store-operated Ca{sup 2+} entry (SOCE). In the absence of external Ca{sup 2+}, the robust Ca{sup 2+}more » entry after subsequent addition of Ca{sup 2+} was decreased by capsaicin in CPA-activated cells. Capsaicin alone increased the actin cytoskeleton, and also increased the actin filament content in cell activation with CPA. These results indicate that capsaicin activates a TRPV1-independent non-SOCE pathway in neutrophils. The reorganization of the actin cytoskeleton is probably involved in the capsaicin inhibition of SOCE.« less

Authors:
 [1];  [2];  [3];  [3];  [4];  [5]
  1. Department of Education and Research, Taichung Veterans General Hospital, 160, Sec. 3, Chung Kang Road, Taichung 407, Taiwan (China) and Graduate Institute of Pharmaceutical Chemistry, School of Pharmacy, Taichung, Taiwan (China). E-mail: w1994@vghtc.gov.tw
  2. Department of Anesthesiology, and Taichung Veterans General Hospital, Taichung, Taiwan (China)
  3. Department of Education and Research, Taichung Veterans General Hospital, 160, Sec. 3, Chung Kang Road, Taichung 407, Taiwan (China)
  4. Department of Pediatrics, Taichung Veterans General Hospital, Taichung, Taiwan (China)
  5. Department of Biochemistry, School of Medicine, China Medical University, Taichung, Taiwan (China)
Publication Date:
OSTI Identifier:
20783377
Resource Type:
Journal Article
Resource Relation:
Journal Name: Toxicology and Applied Pharmacology; Journal Volume: 209; Journal Issue: 2; Other Information: DOI: 10.1016/j.taap.2005.04.002; PII: S0041-008X(05)00165-1; Copyright (c) 2005 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved; Country of input: International Atomic Energy Agency (IAEA)
Country of Publication:
United States
Language:
English
Subject:
60 APPLIED LIFE SCIENCES; ACTIN; CALCIUM IONS; DOPAMINE; INOSITOL; LIGANDS; MICROTUBULES; NEUTROPHILS; NITRIC OXIDE; PYRROLES; RATS; RECEPTORS; RIBOSE; RUTHENIUM; SODIUM IONS

Citation Formats

Wang, J.-P., Tseng, C.-S., Sun, S.-P., Chen, Y.-S., Tsai, C.-R., and Hsu, M.-F. Capsaicin stimulates the non-store-operated Ca{sup 2+} entry but inhibits the store-operated Ca{sup 2+} entry in neutrophils. United States: N. p., 2005. Web. doi:10.1016/j.taap.2005.04.002.
Wang, J.-P., Tseng, C.-S., Sun, S.-P., Chen, Y.-S., Tsai, C.-R., & Hsu, M.-F. Capsaicin stimulates the non-store-operated Ca{sup 2+} entry but inhibits the store-operated Ca{sup 2+} entry in neutrophils. United States. doi:10.1016/j.taap.2005.04.002.
Wang, J.-P., Tseng, C.-S., Sun, S.-P., Chen, Y.-S., Tsai, C.-R., and Hsu, M.-F. Thu . "Capsaicin stimulates the non-store-operated Ca{sup 2+} entry but inhibits the store-operated Ca{sup 2+} entry in neutrophils". United States. doi:10.1016/j.taap.2005.04.002.
@article{osti_20783377,
title = {Capsaicin stimulates the non-store-operated Ca{sup 2+} entry but inhibits the store-operated Ca{sup 2+} entry in neutrophils},
author = {Wang, J.-P. and Tseng, C.-S. and Sun, S.-P. and Chen, Y.-S. and Tsai, C.-R. and Hsu, M.-F.},
abstractNote = {Rat neutrophils express the mRNA encoding for transient receptor potential (TRP) V1. However, capsaicin-stimulated [Ca{sup 2+}]{sub i} elevation occurred only at high concentrations ({>=}100 {mu}M). This response was substantially decreased in a Ca{sup 2+}-free medium. Vanilloids displayed similar patterns of Ca{sup 2+} response with the rank order of potency as follows: scutigeral>resiniferatoxin>capsazepine>capsaicin=olvanil>isovelleral. Arachidonyl dopamine (AAD), an endogenous ligand for TRPV1, failed to desensitize the subsequent capsaicin challenge. Capsaicin-induced Ca{sup 2+} response was not affected by 8-bromo-cyclic ADP-ribose (8-Br-cADPR), the ryanodine receptor blocker, but was slightly attenuated by 1-[6-[17{beta}-3-methoxyestra-1,3,5(10)-trien-17-yl]amino]hexyl]-1H-pyrrole-2,= 5-dione (U-73122), the inhibitor of phospholipase C-coupled processes, 1-[{beta}-[3-(4-methoxyphenyl)propoxy]-4-methoxyphenethyl]-1H-imidazole (SKF-96365), the blocker of receptor-gated and store-operated Ca{sup 2+} (SOC) channels, 2-aminoethyldiphenyl borate (2-APB), the blocker of D-myo-inositol 1,4,5-trisphospahte (IP{sub 3}) receptor and Ca{sup 2+} influx, and by ruthenium red, a blocker of TRPV channels, and enhanced by the Ca{sup 2+} channels blocker, cis-N-(2-phenylcyclopentyl)azacyclotridec-1-en-2-amine (MDL-12330A) and Na{sup +}-deprivation. In addition, capsaicin had no effect on the plasma membrane Ca{sup 2+}-ATPase activity or the production of nitric oxide (NO) and reactive oxygen intermediates (ROI) or on the total thiols content. Capsaicin ({>=}100 {mu}M) inhibited the cyclopiazonic acid (CPA)-induced store-operated Ca{sup 2+} entry (SOCE). In the absence of external Ca{sup 2+}, the robust Ca{sup 2+} entry after subsequent addition of Ca{sup 2+} was decreased by capsaicin in CPA-activated cells. Capsaicin alone increased the actin cytoskeleton, and also increased the actin filament content in cell activation with CPA. These results indicate that capsaicin activates a TRPV1-independent non-SOCE pathway in neutrophils. The reorganization of the actin cytoskeleton is probably involved in the capsaicin inhibition of SOCE.},
doi = {10.1016/j.taap.2005.04.002},
journal = {Toxicology and Applied Pharmacology},
number = 2,
volume = 209,
place = {United States},
year = {Thu Dec 01 00:00:00 EST 2005},
month = {Thu Dec 01 00:00:00 EST 2005}
}