NDLI: Receptor-induced depletion of phosphatidylinositol 4,5-bisphosphate inhibits inwardly rectifying K+ channels in a receptor-specific manner

Content Provider	PubMed Central
Author	Cho, Hana Lee, Doyun Lee, Suk Ho Ho, Won-kyung
Copyright Year	2005
Abstract	Phosphatidylionsitol 4,5-bisphosphate (PIP2), a substrate of phospholipase C, has recently been recognized to regulate membrane-associated proteins and act as a signal molecule in phospholipase C-linked Gq-coupled receptor (GqPCR) pathways. However, it is not known whether PIP2 depletion induced by GqPCRs can act as receptor-specific signals in native cells. We investigated this issue in cardiomyocytes where PIP2-dependent ion channels, G protein-gated inwardly rectifying K+ (GIRK) and inwardly rectifying background K+ (IRK) channels, and various GqPCRs are present. The GIRK current was recorded by using the patch-clamp technique during the application of 10 μM acetylcholine. The extent of receptor-mediated inhibition was estimated as the current decrease over 4 min while taking the GIRK current (I GIRK) value during a previous stimulation as the control. Each GqPCR agonist inhibited I GIRK with different potencies and kinetics. The extents of inhibition induced by phenylephrine, angiotensin II, endothelin-1, prostaglandin F2α, and bradykinin at supramaximal concentrations were (mean ± SE) 32.1 ± 0.6%, 21.9 ± 1.4%, 86.4 ± 1.6%, 63.7 ± 4.9%, and 5.7 ± 1.9%, respectively. GqPCR-induced inhibitions of I GIRK were not affected by protein kinase C inhibitor (calphostin C) but potentiated and became irreversible when the replenishment of PIP2 was blocked by wortmannin (phosphatidylinositol kinase inhibitor). Loading the cells with PIP2 significantly reduced endothelin-1 and prostaglandin F2α-induced inhibition of I GIRK. On the contrary, GqPCR-mediated inhibitions of inwardly rectifying background K+ currents were observed only when GqPCR agonists were applied with wortmannin, and the effects were not parallel with those on I GIRK. These results indicate that GqPCR-induced inhibition of ion channels by means of PIP2 depletion occurs in a receptor-specific manner.
Related Links	http://dx.doi.org/10.1073/pnas.0408844102
Ending Page	4648
Page Count	6
Starting Page	4643
File Format	PDF
ISSN	00278424
e-ISSN	10916490
Journal	Proceedings of the National Academy of Sciences of the United States of America
Issue Number	12
Volume Number	102
Language	English
Publisher	National Academy of Sciences
Publisher Date	2005-03-22
Access Restriction	Open
Rights Holder	National Academy of Sciences
Subject Keyword	General Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Multidisciplinary

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