PMID- 9633531
OWN - NLM
STAT- MEDLINE
DCOM- 19980708
LR  - 20131121
IS  - 0014-4827 (Print)
IS  - 0014-4827 (Linking)
VI  - 241
IP  - 1
DP  - 1998 May 25
TI  - Differential regulation of cyclooxygenases 1 and 2 by interleukin-1 beta, tumor 
      necrosis factor-alpha, and transforming growth factor-beta 1 in human lung 
      fibroblasts.
PG  - 222-9
AB  - In the present studies we found that incubation of human lung fibroblasts with 
      transforming growth factor-beta 1 (TGF-beta 1) potentiated the interleukin-1 beta 
      (IL-1 beta) and/or tumor necrosis factor-alpha (TNF-alpha)-stimulated production 
      of prostaglandin E2 (PGE2). Analysis of fibroblast proteins showed the induction 
      of cyclooxygenase-1 (Cox-1) by TGF-beta 1 and the induction of Cox-2 by IL-1 beta 
      and TNF-alpha. The levels of transcripts for Cox-1 were minimally modified by 
      IL-1 beta or TNF-alpha, however, they were increased by 12-fold by TGF-beta 1. 
      Transcripts for Cox-2 were induced by IL-1 beta or TNF-alpha and their induction 
      was potentiated by TGF-beta 1. TGF-beta 1 alone did not induce Cox-2 transcripts. 
      In vitro transcription assays showed that IL-1 beta and TNF-alpha increased the 
      transcription of the Cox-2 gene, whereas TGF-beta 1 had no effect. Addition of 
      TGF-beta did not increase further the transcription of Cox-2 in IL-1 beta-treated 
      cells, but increased the stability of the corresponding transcripts. The 
      transcription rate of the Cox-1 gene was not increased by any of the cytokines 
      studied. In summary, we demonstrate that the potentiation of PGE2 production by 
      TGF-beta 1 in IL-1 beta and TNF-alpha-treated fibroblasts is the result of 
      transcriptional stimulation of the Cox-2 gene by IL-1 beta and TNF-alpha and the 
      stabilization of the resulting transcripts by TGF-beta 1.
FAU - Diaz, A
AU  - Diaz A
AD  - Department of Medicine, Jefferson Medical College, Thomas Jefferson University, 
      Philadelphia, Pennsylvania 19107, USA.
FAU - Chepenik, K P
AU  - Chepenik KP
FAU - Korn, J H
AU  - Korn JH
FAU - Reginato, A M
AU  - Reginato AM
FAU - Jimenez, S A
AU  - Jimenez SA
LA  - eng
GR  - AR19616/AR/NIAMS NIH HHS/United States
GR  - HL03159/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Exp Cell Res
JT  - Experimental cell research
JID - 0373226
RN  - 0 (Interleukin-1)
RN  - 0 (Isoenzymes)
RN  - 0 (Membrane Proteins)
RN  - 0 (RNA, Messenger)
RN  - 0 (Transforming Growth Factor beta)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - EC 1.14.99.1 (Cyclooxygenase 1)
RN  - EC 1.14.99.1 (Cyclooxygenase 2)
RN  - EC 1.14.99.1 (PTGS1 protein, human)
RN  - EC 1.14.99.1 (PTGS2 protein, human)
RN  - EC 1.14.99.1 (Prostaglandin-Endoperoxide Synthases)
RN  - K7Q1JQR04M (Dinoprostone)
SB  - IM
MH  - Cells, Cultured
MH  - Cyclooxygenase 1
MH  - Cyclooxygenase 2
MH  - Dinoprostone/metabolism
MH  - Female
MH  - Fibroblasts/cytology/drug effects/enzymology
MH  - Gene Expression Regulation, Enzymologic
MH  - Humans
MH  - Interleukin-1/*pharmacology
MH  - Isoenzymes/*drug effects/genetics
MH  - Lung/cytology/*drug effects/enzymology
MH  - Membrane Proteins
MH  - Middle Aged
MH  - Prostaglandin-Endoperoxide Synthases/*drug effects/genetics
MH  - RNA, Messenger/drug effects/metabolism
MH  - Transcription, Genetic/drug effects/genetics
MH  - Transforming Growth Factor beta/*pharmacology
MH  - Tumor Necrosis Factor-alpha/*pharmacology
EDAT- 1998/06/20 00:00
MHDA- 1998/06/20 00:01
CRDT- 1998/06/20 00:00
PHST- 1998/06/20 00:00 [pubmed]
PHST- 1998/06/20 00:01 [medline]
PHST- 1998/06/20 00:00 [entrez]
AID - S0014-4827(98)94050-2 [pii]
AID - 10.1006/excr.1998.4050 [doi]
PST - ppublish
SO  - Exp Cell Res. 1998 May 25;241(1):222-9. doi: 10.1006/excr.1998.4050.