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Basal and UV-induced MMP-1 expression are inhibited by p53 in human dermal fibroblasts

Cited 9 time in Web of Science Cited 9 time in Scopus
Authors

Kim, Sangmin; Lee, Youngae; Lee, Dong Hun; Kim, Yoonkyung; Cho, Kwang Hyun; Chung, Jin Ho

Issue Date
2008-06-19
Publisher
Wiley-Blackwell
Citation
Exp Dermatol. 2008; 17(11): 939-945
Keywords
Adenoviridae/geneticsBenzothiazoles/pharmacologyBlotting, WesternCells, CulturedDermis/cytology/metabolismEtoposide/pharmacologyFibroblasts/drug effects/*metabolism/radiation effectsHumansMatrix Metalloproteinase 1/*metabolismPhosphorylation/drug effects/radiation effectsProto-Oncogene Proteins c-fos/metabolismProto-Oncogene Proteins c-jun/metabolismToluene/analogs & derivatives/pharmacologyTransduction, GeneticTumor Suppressor Protein p53/genetics/*physiologyYoung AdultUltraviolet Rays
Abstract
Ultraviolet (UV) triggers induction of matrix metalloproteinase-1 (MMP-1) and also induces the rapid appearance of p53 protein in the epidermis and dermal fibroblasts. However, little is known about the role of p53 on MMP-1 expression in human skin. Here, we investigated the effects of p53 on basal and UV-induced MMP-1 in human dermal fibroblasts. To verify the role of p53 on MMP-1 expression, adenoviral p53 (Ad-p53) gene was infected to human dermal fibroblasts. Our results showed that basal and UV-induced MMP-1 expression was prevented by Ad-p53. In contrast, p53 inhibitor, pifithrin-alpha augmented the UV-induced MMP-1 expression. On the other hand, p53 activator, etoposide, decreased the MMP-1 expression in both normal and p53-overexpressed cells. In addition, MMP-1 expression was not changed by etoposide and/or pifithrin-alpha in HaCaT cells, which have mutation of p53. Taken together, we suggest that p53 inhibits basal and UV-induced MMP-1 expression in human dermal fibroblasts.
ISSN
1600-0625 (Electronic)
Language
English
URI
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=18557930

https://hdl.handle.net/10371/67537
DOI
https://doi.org/10.1111/j.1600-0625.2008.00729.x
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