PMID- 11694815
OWN - NLM
STAT- MEDLINE
DCOM- 20011213
LR  - 20171101
IS  - 0025-7931 (Print)
IS  - 0025-7931 (Linking)
VI  - 68
IP  - 5
DP  - 2001
TI  - Fibrogenic and inflammatory cytokines modulate mRNA expressions of matrix 
      metalloproteinase-3 and tissue inhibitor of metalloproteinase-3 in type II 
      pneumocytes.
PG  - 509-16
AB  - BACKGROUND: Imbalance between proteinases and their inhibitors released from 
      alveolar type II pneumocytes may cause development of inflammatory lung diseases. 
      OBJECTIVES AND METHODS: We examined mRNA expressions of matrix 
      metalloproteinase-3 (MMP-3) and tissue inhibitor of metalloproteinase-3 (TIMP-3) 
      in a cell line (A549) and in primary culture of normal adult human type II 
      pneumocytes using reverse transcription-competitive polymerase chain reaction. 
      RESULTS: Interleukin-1beta (IL-1beta) and transforming growth factor-beta1 
      (TGF-beta1) increased MMP-3 and TIMP-3 expressions in A549 cells in a time- and 
      concentration-dependent manner. IL-1beta mainly augmented MMP-3 expression, while 
      TGF-beta1 mainly augmented TIMP-3 expression. Dexamethasone attenuated both 
      IL-1beta- and TGF-beta1-stimulated expressions of MMP-3 and TIMP-3. 
      Interleukin-10 had no significant effect. Hepatocyte growth factor alone had no 
      effect on constitutive MMP-3 expression or TIMP-3 expression, but it augmented 
      TGF-beta1-stimulated MMP-3 expression. The constitutive expressions were higher 
      in normal type II pneumocytes than in A549 cells, but the regulations were 
      similar. CONCLUSIONS: These data indicated that the matrix degradation is 
      enhanced by IL-1beta and suppressed by TGF-beta1 via regulations in the balance 
      between MMP-3 and TIMP-3. Further, these regulations were shown to be modulated 
      by glucocorticoids and growth factors.
CI  - Copyright 2001 S. Karger AG, Basel
FAU - Hoshino, Y
AU  - Hoshino Y
AD  - Department of Respiratory Medicine, Graduate School of Medicine, Kyoto 
      University, Kyoto, Japan. yuma@kuhp.kyoto-u.ac.jp
FAU - Mio, T
AU  - Mio T
FAU - Nagai, S
AU  - Nagai S
FAU - Ito, I
AU  - Ito I
FAU - Shigematsu, M
AU  - Shigematsu M
FAU - Izumi, T
AU  - Izumi T
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Switzerland
TA  - Respiration
JT  - Respiration; international review of thoracic diseases
JID - 0137356
RN  - 0 (Cytokines)
RN  - 0 (Interleukin-1)
RN  - 0 (Protease Inhibitors)
RN  - 0 (RNA, Messenger)
RN  - 0 (Tissue Inhibitor of Metalloproteinase-3)
RN  - 0 (Transforming Growth Factor beta)
RN  - EC 3.4.24.17 (Matrix Metalloproteinase 3)
SB  - IM
MH  - Adult
MH  - Cells, Cultured
MH  - Cytokines/*pharmacology
MH  - Cytoplasm/*drug effects/*physiology
MH  - Dose-Response Relationship, Drug
MH  - Humans
MH  - Interleukin-1/pharmacology
MH  - Lung/chemistry/*cytology/enzymology
MH  - Matrix Metalloproteinase 3/*drug effects/*genetics
MH  - Protease Inhibitors/pharmacology
MH  - RNA, Messenger/*drug effects/*physiology
MH  - Reference Values
MH  - Time Factors
MH  - Tissue Inhibitor of Metalloproteinase-3/*drug effects/*physiology
MH  - Transforming Growth Factor beta/pharmacology
EDAT- 2001/11/06 10:00
MHDA- 2002/01/05 10:01
CRDT- 2001/11/06 10:00
PHST- 2001/11/06 10:00 [pubmed]
PHST- 2002/01/05 10:01 [medline]
PHST- 2001/11/06 10:00 [entrez]
AID - 50560 [pii]
AID - 10.1159/000050560 [doi]
PST - ppublish
SO  - Respiration. 2001;68(5):509-16. doi: 10.1159/000050560.