ArticleJournal of cell science2010
Regulation of bile canalicular network formation and maintenance by AMP-activated protein kinase and LKB1.
Article in Journal of cell science, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
46 citing papers in PubMed, 96 citations in OpenAlex.
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- Mechanical mechanics-reclaiming a new battlefield for chronic liver disease.Journal of advanced research · 2026Review
- Formation of functional, extended bile canaliculi, and increased bile acid production in sandwich-cultured human cryopreserved hepatocytes using commercially available culture medium.Archives of toxicology · 2024Article
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- Bile Acid Overload Induced by Bile Duct and Portal Vein Ligation Improves Survival after Staged Hepatectomy in Rats.Current medical science · 2023Article
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- Construction of a culture protocol for functional bile canaliculi formation to apply human iPS cell-derived hepatocytes for cholestasis evaluation.Scientific reports · 2022Article
- Harnessing conserved signaling and metabolic pathways to enhance the maturation of functional engineered tissues.NPJ Regenerative medicine · 2022Review
- One-step visualization of natural cell activities in non-labeled living spheroids.Scientific reports · 2022Article
- In Vitro Assay System to Detect Drug-Induced Bile Acid-Dependent Cytotoxicity Using Hepatocytes.Methods in molecular biology (Clifton, N.J.) · 2022Article
- Collagen Sandwich Culture of Primary Hepatocytes for Image-Based Investigations.Methods in molecular biology (Clifton, N.J.) · 2022Article
- Anisotropic expansion of hepatocyte lumina enforced by apical bulkheads.The Journal of cell biology · 2021Article
- SEW2871 attenuates ANIT-induced hepatotoxicity by protecting liver barrier function via sphingosine 1-phosphate receptor-1-mediated AMPK signaling pathway.Cell biology and toxicology · 2021Article
- Bile Acid Toxicity and Protein Kinases.Advances in experimental medicine and biology · 2021Article
- Prospect ofFrontiers in toxicology · 2021Review
- Metformin and glucose starvation decrease the migratory ability of hepatocellular carcinoma cells: targeting AMPK activation to control migration.Scientific reports · 2019Article
- Association ofFrontiers in cellular and infection microbiology · 2019Article
- Functional polarization of human hepatoma HepaRG cells in response to forskolin.Scientific reports · 2018Article
- Efficient functional cyst formation of biliary epithelial cells using microwells for potential bile duct organisation in vitro.Scientific reports · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
AMP-activated protein kinase (AMPK), a cellular metabolic sensor, is essential in energy regulation and metabolism. Hepatocyte polarization during liver development and regeneration parallels increased metabolism. The current study investigates the effects of AMPK and its upstream activator LKB1 on polarity and bile canalicular network formation and maintenance in collagen sandwich cultures of rat hepatocytes. Immunostaining for the apical protein ABCB1 and the tight junction marker occludin demonstrated that canalicular network formation is sequential and is associated with activation of AMPK and LKB1. AMPK and LKB1 activators accelerated canalicular network formation. Inhibition of AMPK or LKB1 by dominant-negative AMPK or kinase-dead LKB1 constructs blocked canalicular network formation. AICAR and 2-deoxyglucose, which activate AMPK, circumvented the inhibitory effect of kinase-dead LKB1 on canalicular formation, indicating that AMPK directly affects canalicular network formation. After the canalicular network was formed, inhibition of AMPK and LKB1 by dominant-negative AMPK or kinase-dead LKB1 constructs resulted in loss of canalicular network, indicating that AMPK and LKB1 also participate in network maintenance. In addition, activation of AMPK and LKB1 prevented low-Ca(2+)-mediated disruption of the canalicular network and tight junctions. These studies reveal that AMPK and its upstream kinase, LKB1, regulate canalicular network formation and maintenance.
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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.