ArticleJournal of hepatology2008
Activation of focal adhesion kinase and JNK contributes to the extracellular matrix and cAMP-GEF mediated survival from bile acid induced apoptosis in rat hepatocytes.
Article in Journal of hepatology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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
7 citing papers in PubMed, 11 citations in OpenAlex.
- A novel drug-like water-soluble small molecule Focal Adhesion Kinase (FAK) activator promotes intestinal mucosal healing.Current research in pharmacology and drug discovery · 2023Article
- Bile Acid Toxicity and Protein Kinases.Advances in experimental medicine and biology · 2021Article
- Small molecule FAK activator promotes human intestinal epithelial monolayer wound closure and mouse ulcer healing.Scientific reports · 2019Article
- Intracellular cAMP Sensor EPAC: Physiology, Pathophysiology, and Therapeutics Development.Physiological reviews · 2018Review
- Serotonin and the 5-HT7 receptor: the link between hepatocytes, IGF-1 and small intestinal neuroendocrine tumors.Cancer science · 2013Article
- INTRACELLULAR SIGNALING BY BILE ACIDS.Journal of bio-science · 2012Article
- Phosphatidylinositol-3-kinase p110γ contributes to bile salt-induced apoptosis in primary rat hepatocytes and human hepatoma cells.Journal of hepatology · 2010Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
BACKGROUND/
aimsAdherence to an extracellular matrix (ECM) rescues hepatocytes from apoptosis, but how hepatocytes adhered to different ECM and respond to apoptotic and cytoprotective stimuli is unknown.
methodsRat hepatocytes were plated on type 1 collagen (CI), laminin (LM) or polylysine (PL) and the amount of apoptosis induced by glycochenodeoxycholate (GCDC), deoxycholate (DCA), Fas ligand or serum withdrawal was determined by Hoechst staining. The response to cytoprotection by cAMP-guanine exchange factor (cAMP-GEF) activation was determined. Kinase activation was determined by immunoblotting with phosphospecific antibodies.
resultsHepatocytes on LM and PL had more apoptosis in response to all apoptotic stimuli. GCDC increased c-jun-N-terminal kinase (JNK) phosphorylation 2-fold in hepatocytes on CI, but 15- and 30-fold in hepatocytes on PL or LM. SP-600125, a JNK inhibitor, prevented LM and PL potentiation of bile acid apoptosis. GCDC induced dephosphorylation of focal adhesion kinase (FAK) was prevented by cAMP-GEF activation. Cytochalasin B which decreased FAK phosphorylation prevented cAMP-GEF cytoprotection.
conclusionsJNK activation augments apoptosis in hepatocytes plated on PL and LM. Decreased FAK phosphorylation as seen in cells treated with bile acids or attached to PL and LM promotes hepatocyte 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.