CNGA2 Contributes to ATP-Induced Noncapacitative Ca2+ Influx in Vascular Endothelial Cells
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AbstractBackground/Aims: ATP can activate several Ca2+ influx channels in vascular endothelial cells. For example, it stimulates TRPC channels via capacitative and noncapacitative Ca2+ entry (CCE and non-CCE, respectively) mechanisms; it also directly acts on P2X purinoceptors, resulting in Ca2+ influx. In the present study, we tested the hypothesis that cyclic nucleotide-gated (CNG) channels also contribute to ATP-induced non-CCE. Methods: Two selective inhibitors of CNG channels, L-cis-diltiazem and LY-83583, and CNGA2-specific siRNA were used to study the involvement of CNGA2 in ATP-induced non-CCE in endothelial cells. Ca2+ influx was studied using Ca2+-sensitive fluorescence dyes Fluo-3 and Fluo-4. Results/Conclusion: L-cis-diltiazem and LY-83583 markedly reduced ATP-induced non-CCE in 3 types of endothelial cells including the H5V endothelial cell line, the primary cultured bovine aortic endothelial cells and the endothelial cells within isolated mouse aortic strips. The CNGA2-specific siRNA also reduced the ATP-induced non-CCE in H5V endothelial cells. The Ca2+ influx was inhibited by Rp-8-CPT-cAMPS, MDL-12330A, SQ-22536 and MRS-2179, but not by ODQ or NF-157. Taken together, the present study demonstrated that CNGA2 channels contribute to ATP-induced non-CCE in vascular endothelial cells. It is likely that ATP acts through P2Y(1) receptors and adenylyl cyclases to stimulate CNGA2. Copyright (C) 2009 S. Karger AG, Basel
All Author(s) ListKwan HY, Cheng KT, Ma Y, Huang Y, Tang NL, Yu S, Yao XQ
Journal nameJournal of Vascular Research
Year2010
Month1
Day1
Volume Number47
Issue Number2
PublisherKARGER
Pages148 - 156
ISSN1018-1172
eISSN1423-0135
LanguagesEnglish-United Kingdom
KeywordsATP; Ca2+; cAMP; CNGA2 channels; Endothelial cells
Web of Science Subject CategoriesCardiovascular System & Cardiology; Peripheral Vascular Disease; PERIPHERAL VASCULAR DISEASE; Physiology; PHYSIOLOGY

Last updated on 2020-13-08 at 02:17