PGE2 causes a coordinate decrease in the steady state levels of fibronectin and types I and III procollagen mRNAs in normal human dermal fibroblasts.
Prostaglandin E2 (PGE2) caused inhibition of collagen and fibronectin synthesis by confluent cultures of human dermal fibroblasts. Dot-blot hybridization to cDNA probes complementary to Types I and III procollagens and fibronectin demonstrated that inhibition of protein production was accompanied by a coordinate decrease in the steady-state levels of the corresponding mRNAs. Blockade of transcription by actinomycin D demonstrated that PGE2 did not alter the stability of these mRNA. These results indicate that PGE2 is capable of exerting modulation of extracellular matrix biosynthesis, and that these effects occur at a transcriptional level.
D002478:Cells, Cultured; D015232:Dinoprostone; D005109:Extracellular Matrix / Q000378:metabolism; D005347:Fibroblasts / Q000502:physiology; D005353:Fibronectins / Q000235:genetics*; D005786:Gene Expression Regulation / Q000187:drug effects; D006801:Humans; D011347:Procollagen / Q000235:genetics*; D011458:Prostaglandins E / Q000494:pharmacology*; D012333:RNA, Messenger / Q000378:metabolism; D012867:Skin; D014158:Transcription, Genetic / Q000187:drug effects
D005353:Fibronectins; D011347:Procollagen; D011458:Prostaglandins E; D012333:RNA, Messenger; D015232:Dinoprostone