Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2008-2-1
pubmed:abstractText
Ultraviolet (UV) B causes oxidative stress, which has been implicated in carcinogenesis. We determined if the sensitivity of keratinocytes to UVB-induced oxidative stress is dependent on their differentiation state. In primary cultures of undifferentiated and differentiated mouse keratinocytes, UVB (25 mJ/cm(2)) stimulated production of reactive oxygen intermediates. This was associated with increased messenger RNA (mRNA) expression of the antioxidant enzymes glutathione peroxidase, heme oxygenase-1 (HO-1) and the glutathione S-transferase (GST), GSTA1-2. The effects of UVB on GSTA1-2 were greater in undifferentiated when compared with differentiated cells. UVB also induced GSTM1, but only in undifferentiated cells. In contrast, UVB reduced expression of manganese superoxide dismutase, metallothionein-2, GSTA3 and microsomal glutathione S-transferase (mGST)3 in both cell types, whereas it had no major effects on catalase, copper-zinc superoxide dismutase, GSTP1, mGST1 or mGST2. Of note, levels of GSTA4 mRNA were 4- to 5-fold greater in differentiated relative to undifferentiated cells. Moreover, whereas GSTA4 was induced by UVB in undifferentiated cells, it was inhibited in differentiated cells. UVB activated p38 and c-jun N-terminal kinase mitogen-activated protein (MAP) kinases in both undifferentiated and differentiated keratinocytes. Whereas inhibition of these kinases blocked UVB-induced HO-1 in both cell types, GSTA1-2 and GST-4 were only suppressed in undifferentiated cells. In differentiated keratinocytes, p38 inhibition also suppressed GSTA1-2. In contrast, MAP kinase inhibition had no major effects on UVB-induced suppression of GSTA4 in differentiated cells. These data indicate that UVB-induced alterations in antioxidant expression are differentiation dependent. Moreover, MAP kinases are critical regulators of this response. Alterations in antioxidants are likely to be important mechanisms for protecting the skin from UVB-induced oxidative stress.
pubmed:grant
http://linkedlifedata.com/resource/pubmed/grant/AR055073, http://linkedlifedata.com/resource/pubmed/grant/CA093798, http://linkedlifedata.com/resource/pubmed/grant/CA100994, http://linkedlifedata.com/resource/pubmed/grant/ES004738, http://linkedlifedata.com/resource/pubmed/grant/ES005022, http://linkedlifedata.com/resource/pubmed/grant/GM034310, http://linkedlifedata.com/resource/pubmed/grant/R01 CA132624-01, http://linkedlifedata.com/resource/pubmed/grant/R01 CA132624-02, http://linkedlifedata.com/resource/pubmed/grant/R01 ES004738-16A2, http://linkedlifedata.com/resource/pubmed/grant/R01 ES004738-17, http://linkedlifedata.com/resource/pubmed/grant/R01 GM034310-23, http://linkedlifedata.com/resource/pubmed/grant/R01 GM034310-24, http://linkedlifedata.com/resource/pubmed/grant/U54AR055073
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
1460-2180
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
29
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
219-25
pubmed:dateRevised
2011-5-24
pubmed:meshHeading
pubmed:year
2008
pubmed:articleTitle
Distinct effects of ultraviolet B light on antioxidant expression in undifferentiated and differentiated mouse keratinocytes.
pubmed:affiliation
Department of Pharmacology and Toxicology, Rutgers University, 170 Frelinghuysen Road, Piscataway, NJ 08854, USA.
pubmed:publicationType
Journal Article, Research Support, N.I.H., Extramural