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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2-3
pubmed:dateCreated
2009-1-12
pubmed:abstractText
Histamine plays an important role in many physiological functions; and a change in cytosolic Ca(2+) ([Ca(2+)](i)) may be an early signal in these processes. In the present study, we investigated the activation mechanism of TRPC3, the Canonical Transient Receptors Potential 3 Channels, by histamine via a non-capacitative Ca(2+) entry pathway. TRPC3 was transfected into HEK293 cells and the cells were treated with thapsigargin to deplete the intracellular Ca(2+) stores; re-addition of Ca(2+) initiated a capacitative Ca(2+) entry (CCE). A subsequent application of histamine evoked another Ca(2+) influx on top of the CCE signal only in the TRPC3-transfected HEK293 cells, indicating that histamine can activate TRPC3 via a non-capacitative Ca(2+) entry pathway (non-CCE). This histamine-induced non-CCE was abolished by cimitidine, a histamine H(2) receptors antagonist, but not by histamine H(1) receptor antagonists pyrilamine and diphenhydramine. KT5720, a protein kinase A (PKA) inhibitor, had no effect on the histamine-induced non-CCE. This histamine-induced non-CCE was partially reduced by U73122, a phospholipase C (PLC) inhibitor, and by butan-1-ol, a phospholipase D (PLD) inhibitor. When both PLC and PLD inhibitors were simultaneously applied, the non-CCE signal was completely abolished. Taken together, our results showed, for the first time, that histamine could activate TRPC3 via histamine H(2) receptors, and both PLC and PLD participated in this process.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
1879-0712
pubmed:author
pubmed:issnType
Electronic
pubmed:day
14
pubmed:volume
602
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
181-7
pubmed:meshHeading
pubmed:year
2009
pubmed:articleTitle
Stimulation of histamine H2 receptors activates TRPC3 channels through both phospholipase C and phospholipase D.
pubmed:affiliation
Faculty of Medicine, Li Ka Shing Institute of Health Sciences, The Chinese University of Hong Kong, Hong Kong, China. kwanhy@alumni.cuhk.net
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't