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Article: Hepatic tight junctions: From viral entry to cancer metastasis

TitleHepatic tight junctions: From viral entry to cancer metastasis
Authors
KeywordsBile canaliculi
Blood-biliary barrier
Hepatitis
Hepatocytes
Liver neoplasms
Liver steatosis
Tight junctions
Issue Date2010
PublisherBaishideng Publishing Group. The Journal's web site is located at http://www.wjgnet.com/1007-9327/index.htm
Citation
World Journal Of Gastroenterology, 2010, v. 16 n. 3, p. 289-295 How to Cite?
AbstractThe tight junction (TJ) is a critical cellular component for maintenance of tissue integrity, cellular interactions and cell-cell communications, and physiologically functions as the "great wall" against external agents and the surrounding hostile environment. During the host-pathogen evolution, viruses somehow found the key to unlock the gate for their entry into cells and to exploit and exhaust the host cells. In the liver, an array of TJ molecules is localized along the bile canaliculi forming the blood-biliary barrier, where they play pivotal roles in paracellular permeability, bile secretion, and cell polarity. In pathology, certain hepatic TJ molecules mediate virus entry causing hepatitis infection; deregulation and functional abnormality of the TJ have also been implicated in triggering liver cancer development and metastasis. All these findings shed new insights on the understanding of hepatic TJs in the development of liver disease and provide new clues for potential intervention. © 2010 Baishideng. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/83712
ISSN
2015 Impact Factor: 2.787
2015 SCImago Journal Rankings: 1.076
PubMed Central ID
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLee, NPen_HK
dc.contributor.authorLuk, JMen_HK
dc.date.accessioned2010-09-06T08:44:19Z-
dc.date.available2010-09-06T08:44:19Z-
dc.date.issued2010en_HK
dc.identifier.citationWorld Journal Of Gastroenterology, 2010, v. 16 n. 3, p. 289-295en_HK
dc.identifier.issn1007-9327en_HK
dc.identifier.urihttp://hdl.handle.net/10722/83712-
dc.description.abstractThe tight junction (TJ) is a critical cellular component for maintenance of tissue integrity, cellular interactions and cell-cell communications, and physiologically functions as the "great wall" against external agents and the surrounding hostile environment. During the host-pathogen evolution, viruses somehow found the key to unlock the gate for their entry into cells and to exploit and exhaust the host cells. In the liver, an array of TJ molecules is localized along the bile canaliculi forming the blood-biliary barrier, where they play pivotal roles in paracellular permeability, bile secretion, and cell polarity. In pathology, certain hepatic TJ molecules mediate virus entry causing hepatitis infection; deregulation and functional abnormality of the TJ have also been implicated in triggering liver cancer development and metastasis. All these findings shed new insights on the understanding of hepatic TJs in the development of liver disease and provide new clues for potential intervention. © 2010 Baishideng. All rights reserved.en_HK
dc.languageengen_HK
dc.publisherBaishideng Publishing Group. The Journal's web site is located at http://www.wjgnet.com/1007-9327/index.htmen_HK
dc.relation.ispartofWorld Journal of Gastroenterologyen_HK
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.subjectBile canaliculien_HK
dc.subjectBlood-biliary barrieren_HK
dc.subjectHepatitisen_HK
dc.subjectHepatocytesen_HK
dc.subjectLiver neoplasmsen_HK
dc.subjectLiver steatosisen_HK
dc.subjectTight junctionsen_HK
dc.subject.meshCell Membrane Permeability - physiology-
dc.subject.meshHepatitis Viruses - pathogenicity-
dc.subject.meshLiver - physiopathology - ultrastructure-
dc.subject.meshLiver Neoplasms - physiopathology-
dc.subject.meshNeoplasm Metastasis - physiopathology-
dc.titleHepatic tight junctions: From viral entry to cancer metastasisen_HK
dc.typeArticleen_HK
dc.identifier.emailLee, NP: nikkilee@hku.hken_HK
dc.identifier.emailLuk, JM: jmluk@hkucc.hku.hken_HK
dc.identifier.authorityLee, NP=rp00263en_HK
dc.identifier.authorityLuk, JM=rp00349en_HK
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.3748/wjg.v16.i3.289en_HK
dc.identifier.pmid20082472-
dc.identifier.pmcidPMC2807947-
dc.identifier.scopuseid_2-s2.0-75349100759en_HK
dc.identifier.hkuros169120en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-75349100759&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume16en_HK
dc.identifier.issue3en_HK
dc.identifier.spage289en_HK
dc.identifier.epage295en_HK
dc.identifier.isiWOS:000273884700002-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridLee, NP=7402722690en_HK
dc.identifier.scopusauthoridLuk, JM=7006777791en_HK

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