國家衛生研究院 NHRI:Item 3990099045/2491

NHRI > National Institute of Environmental Health Sciences > Louis W. Chang(1999-2009) > Periodical Articles > Item 3990099045/2491

Please use this identifier to cite or link to this item: http://ir.nhri.org.tw/handle/3990099045/2491

Title:	Arsenic induces human keratinocyte apoptosis by the FAS/FAS ligand pathway, which correlates with alterations in nuclear factor-kappa B and activator protein-1 activity
Authors:	Liao, WT;Chang, KL;Yu, CL;Chen, GS;Chang, LW;Yu, HS
Contributors:	Division of Environmental Health and Occupational Medicine
Abstract:	Epidemiologic studies demonstrated that long-term exposure to arsenic induces arsenical skin cancers, including Bowen's disease. Immunohistochemically, Bowen's disease shows proliferating and apoptotic characteristics. The transcription factors nuclear factor-kappaB (NF-kappaB) and activator protein-1 (AP-1) functionally regulate cell proliferation, transformation, and apoptosis. To investigate the mechanism of arsenic-induced apoptosis and related alterations in NF-kappaB and AP-1 activity, we exposed cultured human foreskin keratinocytes to different concentrations of sodium arsenite. At lower concentrations (less than or equal to1 muM), arsenic induced keratinocyte proliferation and enhanced both NF-kappaB and AP-1 activity. At higher concentrations (greater than or equal to5 muM), arsenic induced keratinocyte apoptosis by the Fas/Fas ligand (FasL) pathway. At apoptosis induction concentrations, NF-kappaB activity was not enhanced; however, AP-1 activity was further enhanced. These results indicated that upregulation of NF-kappaB at lower arsenic concentrations was correlated with keratinocyte proliferation. In contrast, higher concentrations of arsenic enhanced AP-1 and induced Fas/FasL-associated apoptosis. The concentration-dependent arsenic effects on transcription factors activity can help to clarify the mechanisms in arsenic-induced proliferation and apoptosis in keratinocytes.
Keywords:	Dermatology
Date:	2004-01
Relation:	Journal of Investigative Dermatology. 2004 Jan;122(1):125-129.
Link to:	http://dx.doi.org/10.1046/j.0022-202X.2003.22109.x
JIF/Ranking 2023:	http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=NHRI&SrcApp=NHRI_IR&KeyISSN=0022-202X&DestApp=IC2JCR
Cited Times(WOS):	https://www.webofscience.com/wos/woscc/full-record/WOS:000187891300022
Cited Times(Scopus):	http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=1642534509
Appears in Collections:	[Louis W. Chang(1999-2009)] Periodical Articles

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