ArticleMolecular biology of the cell2006
Rho kinase, myosin-II, and p42/44 MAPK control extracellular matrix-mediated apical bile canalicular lumen morphogenesis in HepG2 cells.
Article in Molecular biology of the cell, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 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
22 citing papers in PubMed, 49 citations in OpenAlex.
- PAR3-mediated coordination of hepatocyte proliferation, maturation, and architecture in liver development and regeneration.Nature communications · 2026Article
- Rapid transcellular hepatic copper depletion by ARBM-101 rescues severe liver damage in Wilson disease rodents.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2025Article
- Impact of HCV Infection on Hepatocyte Polarity and Plasticity.Pathogens (Basel, Switzerland) · 2022Review
- Spermine oxidase promotes bile canalicular lumen formation through acrolein production.Scientific reports · 2017Article
- Rho-kinase/myosin light chain kinase pathway plays a key role in the impairment of bile canaliculi dynamics induced by cholestatic drugs.Scientific reports · 2016Article
- Structural and functional hepatocyte polarity and liver disease.Journal of hepatology · 2015Review
- The unique polarity phenotype of hepatocytes.Experimental cell research · 2014Review
- The effect of physical and chemical cues on hepatocellular function and morphology.International journal of molecular sciences · 2014Article
- Role of tight junctions in signal transduction: an update.EXCLI journal · 2014Review
- Par1b induces asymmetric inheritance of plasma membrane domains via LGN-dependent mitotic spindle orientation in proliferating hepatocytes.PLoS biology · 2013Article
- Par1b links lumen polarity with LGN-NuMA positioning for distinct epithelial cell division phenotypes.The Journal of cell biology · 2013Article
- Hepatocyte polarity.Comprehensive Physiology · 2013Review
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- Regulation of bile canalicular network formation and maintenance by AMP-activated protein kinase and LKB1.Journal of cell science · 2010Article
- Molecular determinants dictating cell surface expression of the human sodium-dependent vitamin C transporter-2 in human liver cells.American journal of physiology. Gastrointestinal and liver physiology · 2010Article
- Regulatory subunit I-controlled protein kinase A activity is required for apical bile canalicular lumen development in hepatocytes.The Journal of biological chemistry · 2009Article
- Polarization restricts hepatitis C virus entry into HepG2 hepatoma cells.Journal of virology · 2009Article
- Knockdown of tight junction protein claudin-2 prevents bile canalicular formation in WIF-B9 cells.Histochemistry and cell biology · 2009Article
- Anchoring of protein kinase A-regulatory subunit IIalpha to subapically positioned centrosomes mediates apical bile canalicular lumen development in response to oncostatin M but not cAMP.Molecular biology of the cell · 2007Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The molecular mechanisms that regulate multicellular architecture and the development of extended apical bile canalicular lumens in hepatocytes are poorly understood. Here, we show that hepatic HepG2 cells cultured on glass coverslips first develop intercellular apical lumens typically formed by a pair of cells. Prolonged cell culture results in extensive organizational changes, including cell clustering, multilayering, and apical lumen morphogenesis. The latter includes the development of large acinar structures and subsequent elongated canalicular lumens that span multiple cells. These morphological changes closely resemble the early organizational pattern during development, regeneration, and neoplasia of the liver and are rapidly induced when cells are cultured on predeposited extracellular matrix (ECM). Inhibition of Rho kinase or its target myosin-II ATPase in cells cultured on glass coverslips mimics the morphogenic response to ECM. Consistently, stimulation of Rho kinase and subsequent myosin-II ATPase activity by lipoxygenase-controlled eicosatetranoic acid metabolism inhibits ECM-mediated cell multilayering and apical lumen morphogenesis but not initial apical lumen formation. Furthermore, apical lumen remodeling but not cell multilayering requires basal p42/44 MAPK activity. Together, the data suggest a role for hepatocyte-derived ECM in the spatial organization of hepatocytes and apical lumen morphogenesis and identify Rho kinase, myosin-II, and MAPK as potentially important players in different aspects of bile canalicular lumen morphogenesis.
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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.