ArticleAmerican journal of physiology. Cell physiology2012
Cholinergic signaling inhibits oxalate transport by human intestinal T84 cells.
Article in American journal of physiology. Cell physiology, 2012. 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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21 citing papers in PubMed, 33 citations in OpenAlex.
- Contributions of the anion exchangers SLC26A1, SLC26A2, SLC26A3, and SLC26A6 to intestinal oxalate transport in human Caco2-BBE cells.Physiological reports · 2026Article
- Autophagy Regulates Putative Anion Transporter 1 Expression in Intestinal Epithelial Cells.Journal of cellular and molecular medicine · 2025Article
- Altered Gut Microbiota as a Potential Risk Factor for Coronary Artery Disease in Diabetes: A Two-Sample Bi-Directional Mendelian Randomization Study.International journal of medical sciences · 2024Article
- Oxalate (dys)Metabolism: Person-to-Person Variability, Kidney and Cardiometabolic Toxicity.Genes · 2023Review
- Sel1-like proteins and peptides are the majorAmerican journal of physiology. Cell physiology · 2023Article
- Oxalate as a potent promoter of kidney stone formation.Frontiers in medicine · 2023Review
- Activation of the PKA signaling pathway stimulates oxalate transport by human intestinal Caco2-BBE cells.American journal of physiology. Cell physiology · 2020Article
- miR-125a-5p: a novel regulator of SLC26A6 expression in intestinal epithelial cells.American journal of physiology. Cell physiology · 2019Article
- Enhanced gastrointestinal passive paracellular permeability contributes to the obesity-associated hyperoxaluria.American journal of physiology. Gastrointestinal and liver physiology · 2019Article
- Adenosinergic signaling inhibits oxalate transport by human intestinal Caco2-BBE cells through the AAmerican journal of physiology. Cell physiology · 2018Article
- Reduced active transcellular intestinal oxalate secretion contributes to the pathogenesis of obesity-associated hyperoxaluria.Kidney international · 2018Article
- Article
- The role of intestinal oxalate transport in hyperoxaluria and the formation of kidney stones in animals and man.Urolithiasis · 2017Review
- N-glycosylation critically regulates function of oxalate transporter SLC26A6.American journal of physiology. Cell physiology · 2016Article
- Size and dose dependent effects of silver nanoparticle exposure on intestinal permeability in an in vitro model of the human gut epithelium.Journal of nanobiotechnology · 2016Article
- Medical and alternative therapies in urinary tract stone disease.World journal of nephrology · 2015Review
- Pediatric primary urolithiasis: Symptoms, medical management and prevention strategies.World journal of nephrology · 2015Article
- PLC-γ directly binds activated c-Src, which is necessary for carbachol-mediated inhibition of NHE3 activity in Caco-2/BBe cells.American journal of physiology. Cell physiology · 2013Article
- Extracellular nucleotides inhibit oxalate transport by human intestinal Caco-2-BBe cells through PKC-δ activation.American journal of physiology. Cell physiology · 2013Article
- Kidney stones: an update on current pharmacological management and future directions.Expert opinion on pharmacotherapy · 2013Review
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3 authors at 2 institutions in 1 country.
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Abstract
Urolithiasis remains a very common disease in Western countries. Seventy to eighty percent of kidney stones are composed of calcium oxalate, and minor changes in urinary oxalate affect stone risk. Intestinal oxalate secretion mediated by anion exchanger SLC26A6 plays a major constitutive role in limiting net absorption of ingested oxalate, thereby preventing hyperoxaluria and calcium oxalate urolithiasis. Using the relatively selective PKC-δ inhibitor rottlerin, we had previously found that PKC-δ activation inhibits Slc26a6 activity in mouse duodenal tissue. To identify a model system to study physiologic agonists upstream of PKC-δ, we characterized the human intestinal cell line T84. Knockdown studies demonstrated that endogenous SLC26A6 mediates most of the oxalate transport by T84 cells. Cholinergic stimulation with carbachol modulates intestinal ion transport through signaling pathways including PKC activation. We therefore examined whether carbachol affects oxalate transport in T84 cells. We found that carbachol significantly inhibited oxalate transport by T84 cells, an effect blocked by rottlerin. Carbachol also led to significant translocation of PKC-δ from the cytosol to the membrane of T84 cells. Using pharmacological inhibitors, we observed that carbachol inhibits oxalate transport through the M(3) muscarinic receptor and phospholipase C. Utilizing the Src inhibitor PP2 and phosphorylation studies, we found that the observed regulation downstream of PKC-δ is partially mediated by c-Src. Biotinylation studies revealed that carbachol inhibits oxalate transport by reducing SLC26A6 surface expression. We conclude that carbachol negatively regulates oxalate transport by reducing SLC26A6 surface expression in T84 cells through signaling pathways including the M(3) muscarinic receptor, phospholipase C, PKC-δ, and c-Src.
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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.