Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
9
pubmed:dateCreated
2005-10-3
pubmed:abstractText
In this study, we demonstrate that N-ethylmaleimide (NEM), a cell permeable thiol-alkylating agent, enhanced the [Ca2+]i rise caused by stimulation with cyclopiazonic acid (CPA), a sarcoplasmic-endoplasmic reticulum Ca2+-ATPase inhibitor, in rat neutrophils. In addition, NEM attenuated the formyl-Met-Leu-Phe (fMLP)-induced [Ca2+]i rise whether NEM was added to cells prior to or after fMLP stimulation. Moreover, application of NEM after fMLP activation in the absence of external Ca2+ inhibited the Ca2+ signal upon addition of Ca2+ to the medium. Similar patterns were also obtained by using 5,5'-dithiobis-(2-nitrobenzoic acid) (DTNB), a cell impermeable dithiol-oxidizing agent, which replaced NEM in the CPA- and fMLP-induced [Ca2+]i rise experiments. Treatment with dithiothreitol (DTT), a cell permeable dithiol-reducing agent, N-acetyl-l-cysteine (NAC), a cell permeable monothiol-reducing agent, and tris-(2-carboxyethyl)phosphine (TCEP), a cell impermeable reductant without a thiol group, all rescued the fMLP-induced Ca2+ signal from NEM. Rat neutrophils express the mRNA encoding for transient receptor potential (TRP) C6, inositol trisphosphate receptor (IP3R) 2 and IP3R3. NEM had no effect on the mitochondrial membrane potential. NEM could restore the polarization and F-actin accumulation of fMLP-treated cells to those of the control. In the absence of external Ca2+, NEM rendered the CPA-induced [Ca2+]i elevation persistently but inhibited the fMLP-induced Ca2+ spike, which was reversed by tris-(2-cyanoethyl)phosphine (TCP), a cell permeable reductant without a thiol group. DTNB did not affect the Ca2+ spike caused by fMLP. These results indicate that through protein thiol oxidation, NEM affects the receptor-activated and the store depletion-derived Ca2+ signals in an opposing manner.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
http://linkedlifedata.com/resource/pubmed/chemical/Actins, http://linkedlifedata.com/resource/pubmed/chemical/Calcium Channels, http://linkedlifedata.com/resource/pubmed/chemical/Dithionitrobenzoic Acid, http://linkedlifedata.com/resource/pubmed/chemical/Ethylmaleimide, http://linkedlifedata.com/resource/pubmed/chemical/Indoles, http://linkedlifedata.com/resource/pubmed/chemical/Inositol 1,4,5-Trisphosphate..., http://linkedlifedata.com/resource/pubmed/chemical/N-Formylmethionine..., http://linkedlifedata.com/resource/pubmed/chemical/Phosphines, http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger, http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Cytoplasmic and Nuclear, http://linkedlifedata.com/resource/pubmed/chemical/Sulfhydryl Compounds, http://linkedlifedata.com/resource/pubmed/chemical/TRPC Cation Channels, http://linkedlifedata.com/resource/pubmed/chemical/Trrp6 protein, rat, http://linkedlifedata.com/resource/pubmed/chemical/cyclopiazonic acid, http://linkedlifedata.com/resource/pubmed/chemical/tris(2-carboxyethyl)phosphine
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0006-2952
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
70
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1320-9
pubmed:dateRevised
2007-7-18
pubmed:meshHeading
pubmed-meshheading:16143313-Actins, pubmed-meshheading:16143313-Animals, pubmed-meshheading:16143313-Calcium Channels, pubmed-meshheading:16143313-Calcium Signaling, pubmed-meshheading:16143313-Dithionitrobenzoic Acid, pubmed-meshheading:16143313-Ethylmaleimide, pubmed-meshheading:16143313-Indoles, pubmed-meshheading:16143313-Inositol 1,4,5-Trisphosphate Receptors, pubmed-meshheading:16143313-Male, pubmed-meshheading:16143313-Membrane Potentials, pubmed-meshheading:16143313-N-Formylmethionine Leucyl-Phenylalanine, pubmed-meshheading:16143313-Neutrophils, pubmed-meshheading:16143313-Phosphines, pubmed-meshheading:16143313-RNA, Messenger, pubmed-meshheading:16143313-Rats, pubmed-meshheading:16143313-Receptors, Cytoplasmic and Nuclear, pubmed-meshheading:16143313-Sulfhydryl Compounds, pubmed-meshheading:16143313-TRPC Cation Channels
pubmed:year
2005
pubmed:articleTitle
Distinct effects of N-ethylmaleimide on formyl peptide- and cyclopiazonic acid-induced Ca2+ signals through thiol modification in neutrophils.
pubmed:affiliation
Department of Biochemistry, School of Medicine, China Medical University, Taichung, Taiwan, ROC.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't