Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: EC:4.1.99.3 (
PRE
)
1,923
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
The present study assessed the molecular mechanism underlying ultraviolet (UV) B radiation-induced inhibition of the expression of the adhesion molecule
ICAM-1
in human antigen-presenting cells (APC). UVB radiation-induced inhibition of ICAM-I expression in human peripheral blood monocytes was associated with the generation of cyclobutane pyrimidine dimers (CPD). CPD were reduced by 60% after treatment with liposomal packed
photolyase
, an enzyme which removes CPD after absorption of photoreactivating light. Although incomplete, reduction of CPD was associated with complete restoration of
ICAM-1
expression at the mRNA and protein level. Neither reduction of CPD level nor restoration of
ICAM-1
expression were observed, if monocytes were treated with empty liposomes, or if they were irradiated with photoreactivating light prior to application of
photolyase
. DNA damage might also induce soluble mediators capable of autocrine inhibition of
ICAM-1
expression. UVB irradiation of monocytes did not induce IL-10 production, but resulted in release of prostaglandin (PG) E2. Treatment of unirradiated monocytes with PGE2 completely inhibited
ICAM-1
expression, thus mimicking the UVB effect. Inhibition of monocytic PGE2 production by indomethacin, however, did not restore
ICAM-1
expression. These results suggest that formation of CPD is necessary and sufficient for UVB radiation-induced inhibition of
ICAM-1
expression. In contrast, PGE2 might serve a paracrine role in UVB radiation-induced immunosuppression.
...
PMID:Inhibition of intercellular adhesio nmolecule-1 (ICAM-1) expression in ultraviolet B-irradiated human antigen-presenting cells is restored after repair of cyclobutane pyrimidine dimers. 1109 10
