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Hepatic response to chronic hypoxia in experimental rat model through HIF-1 alpha, activator protein-1 and NF-kappa B

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dc.contributor.authorLau, Thomas Y.H.
dc.contributor.authorXiao, Jia
dc.contributor.authorLiong, Emily C.
dc.contributor.authorLiao, Linchuan
dc.contributor.authorLeung, Tung-Ming
dc.contributor.authorNanji, Amin A.
dc.contributor.authorFung, Man Lung
dc.contributor.authorTipoe, George L.
dc.date.accessioned2018-03-09T16:02:37Z
dc.date.available2018-03-09T16:02:37Z
dc.date.issued2013
dc.description.abstractChronic liver diseases are commonly associated with tissue hypoxia that may cause inflammation, oxidative stress, liver cell injury and increased nuclear transcriptional regulation. The hepatic response to chronic hypoxia at the molecular level has not yet been clearly understood until now. The aim of this study is to investigate whether nuclear transcription factors [hypoxia-inducible factor-1 (HIF-1α), activator protein-1 (AP-1), nuclear factor-kappa B (NF-κB)] exhibit activity changes during hepatic response to chronic hypoxia. Blood and liver samples were collected from adult Sprague-Dawley rats living in atmospheric air or 10% oxygen for four weeks. Levels of serum alanine aminotransferase (ALT), 8-isoprostane and nitrotyrosine were measured. The activities of nuclear transcription factors and the expression of downstream genes (iNOS, eNOS, ET-1 and VEGF) were measured using RT-PCR, Western blotting and Gel shift analysis. Results showed that serum ALT level, 8-isoprostane level and formation of nitrotyrosine were within normal range at all time-points. In the hypoxic liver, DNAbinding activities of HIF-1α, NF-κB and AP-1 increased significantly. Expression levels of iNOS, VEGF and ET1 progressively increased from day 7 to day 28. eNOS was also elevated in the hypoxic liver. In conclusion, our study suggests that increased activity of HIF-1α, AP-1 and NF-κB may partly play a significant role in the hepatic response to oxidative stress and liver injury under chronic hypoxia. The increased expression of VEGF, ET-1, iNOS and eNOS may be partly due to the compensatory mechanism in the vascular beds of the liver in response to chronic hypoxia.es
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dc.format.extent9es
dc.identifier.citationHistology and histopathology, Vol. 28, n.º 4 (2013)
dc.identifier.issn1699-5848
dc.identifier.issn0213-3911
dc.identifier.urihttp://hdl.handle.net/10201/57128
dc.languageenges
dc.publisherF. Hernández y Juan F. Madrid. Universidad de Murcia. Departamento de Biología Celular e Histologíaes
dc.rightsinfo:eu-repo/semantics/openAccesses
dc.subjectHypoxiaes
dc.subjectNitric oxidees
dc.subject.otherCDU::5 - Ciencias puras y naturales::57 - Biología::576 - Biología celular y subcelular. Citologíaes
dc.subject.otherCDU::6 - Ciencias aplicadas::61 - Medicinaes
dc.titleHepatic response to chronic hypoxia in experimental rat model through HIF-1 alpha, activator protein-1 and NF-kappa Bes
dc.typeinfo:eu-repo/semantics/articlees
dspace.entity.typePublicationes
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Histology and histopathology Vol.28, nº 4 (2013)