ArticleThe Journal of clinical investigation1994
Increases of intracellular magnesium promote glycodeoxycholate-induced apoptosis in rat hepatocytes.
Article in The Journal of clinical investigation, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
53 citing papers in PubMed, 271 citations in OpenAlex.
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- Bile acids and their receptors: modulators and therapeutic targets in liver inflammation.Seminars in immunopathology · 2022Review
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- Mechanisms of Hepatic Cholestatic Drug Injury.Journal of clinical and translational hepatology · 2019Review
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- Mechanisms of bile acid mediated inflammation in the liver.Molecular aspects of medicine · 2017Review
- The impact of sterile inflammation in acute liver injury.Journal of clinical and translational research · 2017Article
- Studies on the mechanisms of bile acid initiated hepatic inflammation in cholestatic liver injury.Inflammation and cell signaling · 2017Article
- The Involvement of MgOxidative medicine and cellular longevity · 2017Review
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- Hydrophobic bile acid apoptosis is regulated by sphingosine-1-phosphate receptor 2 in rat hepatocytes and human hepatocellular carcinoma cells.American journal of physiology. Gastrointestinal and liver physiology · 2016Article
- Bile Acid-Induced Toxicity in HepaRG Cells Recapitulates the Response in Primary Human Hepatocytes.Basic & clinical pharmacology & toxicology · 2016Article
- Therapeutic targets for cholestatic liver injury.Expert opinion on therapeutic targets · 2016Review
- Visualizing changes in mitochondrial MgChemical science · 2015Article
- Critical Factors in the Assessment of Cholestatic Liver Injury In Vitro.Methods in molecular biology (Clifton, N.J.) · 2015Article
- Primary hepatocytes and their cultures in liver apoptosis research.Archives of toxicology · 2014Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Retention of bile salts by the hepatocyte contributes to liver injury during cholestasis. Although cell injury can occur by one of two mechanisms, necrosis versus apoptosis, information is lacking regarding apoptosis as a mechanism of cell death by bile salts. Our aim was to determine if the bile salt glycodeoxycholate (GDC) induces apoptosis in rat hepatocytes. Morphologic assessment included electron microscopy and quantitation of nuclear fragmentation by fluorescent microscopy. Biochemical studies included measurements of DNA fragmentation, in vitro endonuclease activity, cytosolic free Ca2+ (Cai2+), and cytosolic free Mg2+ (Mgi2+). Morphologic studies demonstrated typical features of apoptosis in GDC (50 microM) treated cells. The "ladder pattern" of DNA fragmentation was also present in DNA obtained from GDC-treated cells. In vitro endonuclease activity was 2.5-fold greater with Mg2+ than Ca2+. Although basal Cai2+ values did not change after addition of GDC, Mgi2+ increased twofold. Incubation of cells in an Mg(2+)-free medium prevented the rise in Mgi2+ and reduced nuclear and DNA fragmentation. In conclusion, GDC induces apoptosis in hepatocytes by a mechanism promoted by increases of Mgi2+ with stimulation of Mg(2+)-dependent endonucleases. These data suggest for the first time that changes of Mgi2+ may participate in the program of cellular events culminating in apoptosis.
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Registered trials
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.