PMID- 7514600
OWN - NLM
STAT- MEDLINE
DCOM- 19940622
LR  - 20210210
IS  - 0021-9258 (Print)
IS  - 0021-9258 (Linking)
VI  - 269
IP  - 19
DP  - 1994 May 13
TI  - Insulin-like growth factors, their binding proteins, and transforming growth 
      factor-beta 1 in oxidant-arrested lung alveolar epithelial cells.
PG  - 14111-7
AB  - The epithelium of the pulmonary alveolus is a major target for oxidant injury, 
      and its proper repair following injury is dependent on the proliferative response 
      of its stem cells, the type 2 cells. We have recently shown that hyperoxia 
      arrests proliferation of an immortalized type 2 cell line (SV40T-T2) and that 
      expression of several growth-related genes, normally induced near the G1/S and 
      boundary was altered with a block of translation of their mRNA. In the present 
      study we examined the possible role of the insulin-like growth factor (IGF) 
      system and of transforming growth factor-beta 1 (TGF-beta 1) in the arrest of 
      proliferation induced by hyperoxia. We show that IGF-binding protein 2 (IGFBP-2) 
      accumulates to higher levels in culture medium of SV40T-T2 cells whose 
      proliferation has been arrested by hyperoxia. This proliferation arrest is 
      associated with increased expression of IGFBP-2 mRNA and with induction of type 2 
      IGF receptor and IGF-II mRNAs. When O2-arrested cells were allowed to resume 
      proliferation in normoxia, the level of expression of these genes rapidly 
      decreased to control levels. We also, found that TGF-beta 1 was induced by O2 
      exposure, that TGF-beta 1 inhibited SV40T-T2 proliferation, and that TGF-beta 1 
      itself was a potent stimulator of IGFBP-2 expression. These studies suggest a 
      regulatory link between components of the IGF system and TGF-beta 1 in hyperoxic 
      control of cell proliferation of alveolar epithelial cells.
FAU - Cazals, V
AU  - Cazals V
AD  - Physiology Department, Hospital Trousseau, St. Antoine Medical School, University 
      of Paris.
FAU - Mouhieddine, B
AU  - Mouhieddine B
FAU - Maitre, B
AU  - Maitre B
FAU - Le Bouc, Y
AU  - Le Bouc Y
FAU - Chadelat, K
AU  - Chadelat K
FAU - Brody, J S
AU  - Brody JS
FAU - Clement, A
AU  - Clement A
LA  - eng
GR  - P01-HL47049/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Biol Chem
JT  - The Journal of biological chemistry
JID - 2985121R
RN  - 0 (Carrier Proteins)
RN  - 0 (DNA Primers)
RN  - 0 (Insulin-Like Growth Factor Binding Protein 2)
RN  - 0 (Oxidants)
RN  - 0 (RNA, Messenger)
RN  - 0 (Somatomedins)
RN  - 0 (Transforming Growth Factor beta)
RN  - S88TT14065 (Oxygen)
SB  - IM
MH  - Animals
MH  - Base Sequence
MH  - Carrier Proteins/genetics/*metabolism
MH  - Cell Division/drug effects
MH  - Cells, Cultured
MH  - DNA Primers
MH  - Epithelial Cells
MH  - Epithelium/drug effects/metabolism
MH  - Insulin-Like Growth Factor Binding Protein 2
MH  - Molecular Sequence Data
MH  - Oxidants/*pharmacology
MH  - Oxygen/pharmacology
MH  - Pulmonary Alveoli/cytology/drug effects/*metabolism
MH  - RNA, Messenger/metabolism
MH  - Rats
MH  - Somatomedins/genetics/*metabolism
MH  - Transforming Growth Factor beta/biosynthesis/*metabolism
EDAT- 1994/05/13 00:00
MHDA- 1994/05/13 00:01
CRDT- 1994/05/13 00:00
PHST- 1994/05/13 00:00 [pubmed]
PHST- 1994/05/13 00:01 [medline]
PHST- 1994/05/13 00:00 [entrez]
AID - S0021-9258(17)36761-3 [pii]
PST - ppublish
SO  - J Biol Chem. 1994 May 13;269(19):14111-7.