ArticleBMC cell biology2009
Protein kinase C activation disrupts epithelial apical junctions via ROCK-II dependent stimulation of actomyosin contractility.
Article in BMC cell biology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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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
34 citing papers in PubMed, 51 citations in OpenAlex.
- Exploring the nexus between MYH9 and tumors: novel insights and new therapeutic opportunities.Frontiers in cell and developmental biology · 2024Review
- Unique and redundant functions of cytoplasmic actins and nonmuscle myosin II isoforms at epithelial junctions.Annals of the New York Academy of Sciences · 2022Review
- Inflammation and the Intestinal Barrier: Leukocyte-Epithelial Cell Interactions, Cell Junction Remodeling, and Mucosal Repair.Gastroenterology · 2016Review
- Conditional knockout of polarity complex (atypical) PKCι reveals an anti-inflammatory function mediated by NF-κB.Molecular biology of the cell · 2016Article
- Loss of cortactin causes endothelial barrier dysfunction via disturbed adrenomedullin secretion and actomyosin contractility.Scientific reports · 2016Article
- ROCK inhibition enhances neurite outgrowth in neural stem cells by upregulating YAP expression in vitro.Neural regeneration research · 2016Article
- Nonmuscle Myosin IIA Regulates Intestinal Epithelial Barrier in vivo and Plays a Protective Role During Experimental Colitis.Scientific reports · 2016Article
- Crosstalk between Inflammation and ROCK/MLCK Signaling Pathways in Gastrointestinal Disorders with Intestinal Hyperpermeability.Gastroenterology research and practice · 2016Review
- ROCK2 primes the endothelium for vascular hyperpermeability responses by raising baseline junctional tension.Vascular pharmacology · 2015Article
- Diadenosine tetraphosphate induces tight junction disassembly thus increasing corneal epithelial permeability.British journal of pharmacology · 2015Article
- Proinflammatory cytokine-induced tight junction remodeling through dynamic self-assembly of claudins.Molecular biology of the cell · 2014Article
- Article
- Role of guanine nucleotide exchange factor-H1 in complement-mediated RhoA activation in glomerular epithelial cells.The Journal of biological chemistry · 2014Article
- Phosphatase regulation of intercellular junctions.Tissue barriers · 2013Review
- Characterization of three full-length human nonmuscle myosin II paralogs.The Journal of biological chemistry · 2013Article
- Bile duct epithelial tight junctions and barrier function.Tissue barriers · 2013Review
- Tight junctions in human pancreatic duct epithelial cells.Tissue barriers · 2013Review
- Novel mechanism of cytokine-induced disruption of epithelial barriers: Janus kinase and protein kinase D-dependent downregulation of junction protein expression.Tissue barriers · 2013Article
- Signaling through myosin light chain kinase in smooth muscles.The Journal of biological chemistry · 2013Article
- The digestive neuronal-glial-epithelial unit: a new actor in gut health and disease.Nature reviews. Gastroenterology & hepatology · 2013Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundDisruption of epithelial cell-cell adhesions represents an early and important stage in tumor metastasis. This process can be modeled in vitro by exposing cells to chemical tumor promoters, phorbol esters and octylindolactam-V (OI-V), known to activate protein kinase C (PKC). However, molecular events mediating PKC-dependent disruption of epithelial cell-cell contact remain poorly understood. In the present study we investigate mechanisms by which PKC activation induces disassembly of tight junctions (TJs) and adherens junctions (AJs) in a model pancreatic epithelium.
resultsExposure of HPAF-II human pancreatic adenocarcinoma cell monolayers to either OI-V or 12-O-tetradecanoylphorbol-13-acetate caused rapid disruption and internalization of AJs and TJs. Activity of classical PKC isoenzymes was responsible for the loss of cell-cell contacts which was accompanied by cell rounding, phosphorylation and relocalization of the F-actin motor nonmuscle myosin (NM) II. The OI-V-induced disruption of AJs and TJs was prevented by either pharmacological inhibition of NM II with blebbistatin or by siRNA-mediated downregulation of NM IIA. Furthermore, AJ/TJ disassembly was attenuated by inhibition of Rho-associated kinase (ROCK) II, but was insensitive to blockage of MLCK, calmodulin, ERK1/2, caspases and RhoA GTPase.
conclusionOur data suggest that stimulation of PKC disrupts epithelial apical junctions via ROCK-II dependent activation of NM II, which increases contractility of perijunctional actin filaments. This mechanism is likely to be important for cancer cell dissociation and tumor metastasis.
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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.