ArticleAmerican journal of physiology. Renal physiology2010
Role of TRPC3 channels in ATP-induced Ca2+ signaling in principal cells of the inner medullary collecting duct.
Article in American journal of physiology. Renal physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 29 citations in OpenAlex.
- Sex-specific Stone-forming Phenotype in Mice During Hypercalciuria/Urine Alkalinization.Laboratory investigation; a journal of technical methods and pathology · 2024Article
- TRPC Channels in the Physiology and Pathophysiology of the Renal Tubular System: What Do We Know?International journal of molecular sciences · 2022Review
- Polymodal roles of TRPC3 channel in the kidney.Channels (Austin, Tex.) · 2020Review
- Collecting duct cells show differential retinoic acid responses to acute versus chronic kidney injury stimuli.Scientific reports · 2020Article
- Evidence for a regulated CaJournal of cell science · 2019Article
- TRPC3 determines osmosensitive [Ca2+]i signaling in the collecting duct and contributes to urinary concentration.PloS one · 2019Article
- Kidney Proximal Tubule Lipoapoptosis Is Regulated by Fatty Acid Transporter-2 (FATP2).Journal of the American Society of Nephrology : JASN · 2018Article
- Adenosine AAmerican journal of physiology. Renal physiology · 2017Article
- Potential Mechanisms Underlying Inflammation-Enhanced Aminoglycoside-Induced Cochleotoxicity.Frontiers in cellular neuroscience · 2017Review
- Canonical Transient Receptor Potential 6 Channel: A New Target of Reactive Oxygen Species in Renal Physiology and Pathology.Antioxidants & redox signaling · 2016Review
- Maintaining KAmerican journal of physiology. Renal physiology · 2016Review
- Evidence of a Role for Fibroblast Transient Receptor Potential Canonical 3 Ca2+ Channel in Renal Fibrosis.Journal of the American Society of Nephrology : JASN · 2015Article
- Flow regulation of endothelin-1 production in the inner medullary collecting duct.American journal of physiology. Renal physiology · 2015Article
- Purinergic signalling in the kidney in health and disease.Purinergic signalling · 2014Review
- Article
- Manganese inhibits ATP-induced calcium entry through the transient receptor potential channel TRPC3 in astrocytes.Neurotoxicology · 2013Article
- Extracellular Ca(2+) sensing in salivary ductal cells.The Journal of biological chemistry · 2012Article
- Protein S-glutathionylation enhances Ca2+-induced Ca2+ release via the IP3 receptor in cultured aortic endothelial cells.The Journal of physiology · 2012Article
- Article
- Effect of protein S-glutathionylation on Ca2+ homeostasis in cultured aortic endothelial cells.American journal of physiology. Heart and circulatory physiology · 2011Article
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
The transient receptor potential channel TRPC3 is exclusively expressed in the apical membrane of principal cells of the collecting duct (CD) both in vivo and in the mouse CD cell line IMCD-3. Previous studies revealed that ATP-induced apical-to-basolateral transepithelial Ca(2+) flux across IMCD-3 monolayers is increased by overexpression of TRPC3 and attenuated by a dominant negative TRPC3 construct, suggesting that Ca(2+) entry across the apical membrane occurs via TRPC3 channels. To test this hypothesis, we selectively measured the Ca(2+) permeability of the apical membrane of fura-2-loaded IMCD-3 cells using the Mn(2+) quench technique. Mn(2+) influx across the apical membrane was increased 12- to 16-fold by apical ATP and was blocked by the pyrazole derivative BTP2, a known inhibitor of TRPC3 channels, with an IC(50) value <100 nM. In contrast, Mn(2+) influx was only increased approximately 2-fold by basolateral ATP. Mn(2+) influx was also activated by apical, but not basolateral, 1-stearoyl-2-acetyl-sn-glycerol (SAG), a known activator of TRPC3 channels. Apical ATP- and SAG-induced Mn(2+) influx was increased by overexpression of TRPC3 and completely blocked by expression of the dominant negative TRPC3 construct. Mn(2+) influx was also stimulated approximately 2-fold by thapsigargin applied to either the apical or basolateral side. Thapsigargin-induced flux was blocked by BTP2 but was unaffected by overexpression of TRPC3 or by dominant negative TRPC3. Apical ATP, but not basolateral ATP, increased transepithelial (45)Ca(2+) flux. These results demonstrate that the apical membrane of IMCD-3 cells has two distinct Ca(2+) influx pathways: 1) a store-operated channel activated by thapsigargin and basolateral ATP and 2) TRPC3 channels activated by apical ATP. Only activation of TRPC3 leads to net transepithelial apical-to-basolateral Ca(2+) flux. Furthermore, these results demonstrate that native TRPC3 is not a store-operated channel in IMCD-3 cells.
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