Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1993-6-16
pubmed:abstractText
In human epidermis, basal keratinocytes are the main source of interleukin-1 (IL-1), and IL-1 alpha is the predominant form, whereas IL-1 beta appears to exist predominantly in cultured keratinocytes. We investigated the effects of retinoic acid (RA) treatments on IL-1 alpha and -beta protein and mRNA expression of normal human keratinocytes cultured in low-calcium defined medium with or without hydrocortisone. Radioimmunoassay showed that after stimulation by RA, the IL-1 beta intracellular level is predominantly increased, with no significant modification of IL-1 alpha expression. The addition of hydrocortisone in the culture medium resulted in a decrease in RA-induced IL-1 beta overexpression, without notable modifications in untreated cultures. Release of both IL-1 alpha and -beta in culture supernatants was detectable only after RA treatment and in the absence of hydrocortisone. The overexpression of IL-1 beta in control and RA-treated cultures mainly concerned the 52- and 31- to 36-kD biologically inactive precursor forms. Northern blot using specific IL-1 alpha and -beta oligonucleotide probes showed that IL-1 beta mRNA predominate over IL-1 alpha mRNA and reach a maximal level 6 h before the IL-1 beta protein peak. These findings indicate that in cultured keratinocytes intracellular IL-1 beta is preferentially increased by RA but in its immature forms. The significance of this overexpression remains to be elucidated.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
1011-0283
pubmed:author
pubmed:issnType
Print
pubmed:volume
6
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
10-9
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1993
pubmed:articleTitle
Effects of retinoic acid on interleukin-1 alpha and -1 beta expression by normal human keratinocytes cultured in defined medium.
pubmed:affiliation
INSERM U 346, affiliée CNRS, Pavillon R, Hôpital E.-Herriot, Lyon, France.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't