ArticleBritish journal of pharmacology2012
Pharmacological profile of phosphatidylinositol 3-kinases and related phosphatidylinositols mediating endothelin(A) receptor-operated native TRPC channels in rabbit coronary artery myocytes.
Article in British journal of pharmacology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 15 citations in OpenAlex.
- Role for the PIPJournal of cell communication and signaling · 2024Review
- Obligatory role for PKCδ in PIPThe Journal of physiology · 2020Article
- RNA-seq analysis reveals TRPC genes to impact an unexpected number of metabolic and regulatory pathways.Scientific reports · 2020Article
- Insights into Activation Mechanisms of Store-Operated TRPC1 Channels in Vascular Smooth Muscle.Cells · 2020Review
- ENKUR Is Involved in the Regulation of Cellular Biology in Colorectal Cancer Cells via PI3K/Akt Signaling Pathway.Technology in cancer research & treatment · 2019Article
- Upregulation of Transient Receptor Potential Canonical Channels Contributes to Endotoxin-Induced Pulmonary Arterial Stenosis.Medical science monitor : international medical journal of experimental and clinical research · 2016Article
- Transient receptor potential channels in the vasculature.Physiological reviews · 2015Review
- Role of TRP channels in the cardiovascular system.American journal of physiology. Heart and circulatory physiology · 2015Review
- Myristoylated alanine-rich C kinase substrate coordinates native TRPC1 channel activation by phosphatidylinositol 4,5-bisphosphate and protein kinase C in vascular smooth muscle.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2014Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
background and purposeEndothelin(A) (ET(A) ) receptor-operated canonical transient receptor potential (TRPC) channels mediate Ca²⁺ influx pathways, which are important in coronary artery function. Biochemical pathways linking ET(A) receptor stimulation to TRPC channel opening are unknown. We investigated the involvement of phosphatidylinositol 3-kinases (PI3K) in ET(A) receptor activation of native heteromeric TRPC1/C5/C6 and TRPC3/C7 channels in rabbit coronary artery vascular smooth muscle cells (VSMCs). EXPERIMENTAL APPROACH: A pharmacological profile of PI3K was created by studying the effect of pan-PI3K, pan-Class I PI3K and Class I PI3K isoform-selective inhibitors on ET(A) receptor-evoked single TRPC1/C5/C6 and TRPC3/C7 channel activities in cell-attached patches from rabbit freshly isolated coronary artery VSMCs. The action of phosphatidylinositol 3-phosphate- [PI(3)P], 4-phosphate- [PI(4)P] and 5-phosphate- [PI(5)P] containing molecules involved in PI3K-mediated reactions were studied in inside-out patches. Expression of PI3K family members in coronary artery tissue lysates were analysed using quantitative PCR. KEY
resultsET(A) receptor-operated TRPC1/C5/C6 and TRPC3/C7 channel activities were inhibited by wortmannin. However, ZSTK474 and AS252424 reduced ET(A) receptor-evoked TRPC1/C5/C6 channel activity but potentiated TRPC3/C7 channel activity. All the PI(3)P-, PI(4)P- and PI(5)P-containing molecules tested induced TRPC1/C5/C6 channel activation, whereas only PI(3)P stimulated TRPC3/C7 channels. CONCLUSIONS AND IMPLICATIONS: ET(A) receptor-operated native TRPC1/C5/C6 and TRPC3/C7 channel activities are likely to be mediated by Class I PI3Kγ and Class II/III PI3K isoforms, respectively. ET(A) receptor-evoked and constitutively active PI3Kγ-mediated pathways inhibit TRPC3/C7 channel activation. PI3K-mediated pathways are novel regulators of native TRPC channels in VSMCs, and these signalling cascades are potential pharmacological targets for coronary artery disease.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.