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Responses of murine keratinocytes to oxidative stress

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TitleInfo
Title
Responses of murine keratinocytes to oxidative stress
Name (type = personal)
NamePart (type = family)
Black
NamePart (type = given)
Adrienne T.
DisplayForm
Adrienne Black
Role
RoleTerm (authority = RUETD)
author
Name (type = personal)
NamePart (type = family)
Laskin
NamePart (type = given)
Jeffrey
Affiliation
Advisory Committee
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Jeffrey D Laskin
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chair
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NamePart (type = family)
Laskin
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Debra
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Advisory Committee
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Debra L Laskin
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internal member
Name (type = personal)
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Gerecke
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Donald
Affiliation
Advisory Committee
DisplayForm
Donald R Gerecke
Role
RoleTerm (authority = RULIB)
internal member
Name (type = personal)
NamePart (type = family)
Gordon
NamePart (type = given)
Marion
Affiliation
Advisory Committee
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Marion A Gordon
Role
RoleTerm (authority = RULIB)
internal member
Name (type = personal)
NamePart (type = family)
Heck
NamePart (type = given)
Diane
Affiliation
Advisory Committee
DisplayForm
Diane E Heck
Role
RoleTerm (authority = RULIB)
internal member
Name (type = personal)
NamePart (type = family)
Heindel
NamePart (type = given)
Ned
Affiliation
Advisory Committee
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Ned Heindel
Role
RoleTerm (authority = RULIB)
outside member
Name (type = corporate)
NamePart
Rutgers University
Role
RoleTerm (authority = RULIB)
degree grantor
Name (type = corporate)
NamePart
Graduate School-New Brunswick
Role
RoleTerm (authority = RULIB)
school
TypeOfResource
Text
Genre (authority = marcgt)
theses
OriginInfo
DateCreated (qualifier = exact)
2007
DateOther (qualifier = exact); (type = degree)
2007
Language
LanguageTerm (authority = ISO 639-3:2007); (type = text)
English
PhysicalDescription
Form (authority = marcform)
electronic
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application/pdf
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text/xml
Extent
xvii, 168 pages
Note
Pages missing
Abstract (type = abstract)
Oxidative stress is well recognized as a major contributing factor in the development of cutaneous disease. The generation of reactive oxygen intermediates (ROI) damage cellular macromolecules, causing mutagenic DNA lesions, altered enzyme function, lipid peroxidation and inappropriate signaling. Induction of oxidative stress is associated with the onset of inflammation through production of arachidonic acid-derived lipid mediators including prostaglandins and leukotrienes although the mechanisms linking these two processes are unclear at this time. As the protective barrier of the body, the skin is exposed to many oxidants. Two such potent inducers of oxidative stress are the high energy wavelengths of the ultraviolet B (UVB) spectra (290-320 nm) and the redoxcycling herbicide paraquat (1,1'-dimethyl-4,4'-bipyridinium). In the present studies, we compared the effect of UVB and paraquat on the expression of antioxidant and arachidonic acid metabolism enzymes in undifferentiated and calcium-differentiated primary mouse keratinocytes. Using enzyme assays, we found that both UVB (2.5-25mJ/cm2) and paraquat (100 µM) generated ROI and were effective inducers of oxidative stress in these cells and that paraquat readily undergoes redox-cycling. Both agents upregulated the expression of several antioxidant enzymes, measured using realtime PCR although a greater number of enzymes were induced by paraquat. UVB and paraquat equally upregulated eicosanoid enzyme expression; these enzymes included the cyclooxygenases, prostanoid synthases, lipoxygenases and leukotriene synthetic enzymes as well as the prostaglandin and leukotriene receptors. Using HPLC with fluorescence detection, UVB was found to modulate prostaglandin production. In both cell types, UVB caused a dose-dependent activation of the p38 and JNK MAP kinases. Akt kinase, however, was found to be activated only in undifferentiated cells with constitutive phosphorylation in differentiated cells. Inhibition of these enzymes markedly inhibited mRNA expression of several eicosanoid enzymes while other enzymes other were unaffected. Taken together, these data demonstrate that UVB light and paraquat effectively induce both antioxidant and eicosanoid biosynthetic enzymes in mouse keratinocytes and that activation of these pathways are regulated by MAP and Akt kinase activity. The elucidation of the keratinocyte response to oxidative stress is a necessary step to a better understanding of the effects of oxidants on the skin.
Note (type = degree)
Ph.D.
Subject (authority = RUETD)
Topic
Toxicology
Subject (authority = ETD-LCSH)
Topic
Keratinocytes
Subject (authority = ETD-LCSH)
Topic
Mice
RelatedItem (type = host)
TitleInfo
Title
Graduate School - New Brunswick Electronic Theses and Dissertations
Identifier (type = local)
rucore19991600001
Identifier (type = hdl)
http://hdl.rutgers.edu/1782.2/rucore10001600001.ETD.13490
Identifier
ETD_162
Identifier (type = doi)
doi:10.7282/T36W9BJN
Location
PhysicalLocation (authority = marcorg); (displayLabel = Rutgers, The State University of New Jersey)
NjNbRU
Genre (authority = ExL-Esploro)
ETD doctoral
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The author owns the copyright to this work.
Copyright
Status
Copyright protected
Availability
Status
Open
AssociatedEntity (AUTHORITY = rulib); (ID = 1)
Name
Adrienne Black
Role
Copyright holder
Affiliation
Rutgers University. Graduate School-New Brunswick
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Permission or license
Detail
Non-exclusive ETD license
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License
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Author Agreement License
Detail
I hereby grant to the Rutgers University Libraries and to my school the non-exclusive right to archive, reproduce and distribute my thesis or dissertation, in whole or in part, and/or my abstract, in whole or in part, in and from an electronic format, subject to the release date subsequently stipulated in this submittal form and approved by my school. I represent and stipulate that the thesis or dissertation and its abstract are my original work, that they do not infringe or violate any rights of others, and that I make these grants as the sole owner of the rights to my thesis or dissertation and its abstract. I represent that I have obtained written permissions, when necessary, from the owner(s) of each third party copyrighted matter to be included in my thesis or dissertation and will supply copies of such upon request by my school. I acknowledge that RU ETD and my school will not distribute my thesis or dissertation or its abstract if, in their reasonable judgment, they believe all such rights have not been secured. I acknowledge that I retain ownership rights to the copyright of my work. I also retain the right to use all or part of this thesis or dissertation in future works, such as articles or books.
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