PMID- 9042152
OWN - NLM
STAT- MEDLINE
DCOM- 19970318
LR  - 20061115
IS  - 0023-6837 (Print)
IS  - 0023-6837 (Linking)
VI  - 76
IP  - 2
DP  - 1997 Feb
TI  - P53 and p21 (Waf1/Cip1) mRNA expression associated with DNA damage and repair in 
      acute immune complex alveolitis in mice.
PG  - 161-9
AB  - The tumor suppresser p53 is a cell cycle checkpoint protein that contributes to 
      the preservation of genetic stability by mediating either a G1 arrest or 
      apoptosis in response to DNA damage. p53 causes growth arrest through 
      transcriptional activation of the cyclin-dependent kinase inhibitor p21. During 
      p53-mediated suppression of cell proliferation, p21 is important for coordinating 
      cell cycle progression, DNA replication, and repair of damaged DNA. The purpose 
      of this study is to investigate the expression of p53 and p21 mRNA in association 
      with DNA damage and normal repair in acute immune complex alveolitis in mice. 
      Male ICR mice were injected intravenously with IgG antibodies against oval 
      albumin, aerosolized with oval albumin solution, and killed at 4, 6, 12, 24, and 
      48 hours and 1 week after aerosolization. We assessed the expression of p53 and 
      p21 mRNA by reverse transcriptase (RT)-PCR and by RT in situ PCR. We also 
      assessed DNA damage by terminal deoxynucleotidyl transferase mediated biotin-dUTP 
      nick-end-labeling (TUNEL) and by gel electrophoresis of DNA extracted from lung 
      tissues. The results of RT-PCR and RT in situ PCR showed that p53 and p21 mRNA 
      were concurrently up-regulated at 4 to 48 hours after aerosolization in alveolar 
      epithelial cells. Bronchial and alveolar epithelial cells were positively stained 
      by TUNEL in this period but not at 1 week after aerosolization or in control 
      mice. The result of electrophoretic analysis of DNA was compatible with that of 
      TUNEL. These studies suggest that the responses of p53 and p21 mRNA are 
      associated with physiologic processes of DNA damage and repair in acute immune 
      complex alveolitis in mice.
FAU - Kuwano, K
AU  - Kuwano K
AD  - Research Institute for Diseases of the Chest, Faculty of Medicine, Kyushu 
      University, Fukuoka, Japan.
FAU - Hagimoto, N
AU  - Hagimoto N
FAU - Nomoto, Y
AU  - Nomoto Y
FAU - Kawasaki, M
AU  - Kawasaki M
FAU - Kunitake, R
AU  - Kunitake R
FAU - Fujita, M
AU  - Fujita M
FAU - Miyazaki, H
AU  - Miyazaki H
FAU - Hara, N
AU  - Hara N
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Lab Invest
JT  - Laboratory investigation; a journal of technical methods and pathology
JID - 0376617
RN  - 0 (Cdkn1a protein, mouse)
RN  - 0 (Cyclin-Dependent Kinase Inhibitor p21)
RN  - 0 (Cyclins)
RN  - 0 (RNA, Messenger)
SB  - IM
MH  - Animals
MH  - Apoptosis
MH  - Cyclin-Dependent Kinase Inhibitor p21
MH  - Cyclins/*genetics
MH  - Genes, p53/*genetics
MH  - *Immune Complex Diseases
MH  - In Situ Hybridization
MH  - Lung/pathology
MH  - Male
MH  - Mice
MH  - Mice, Inbred ICR
MH  - Molecular Biology
MH  - Polymerase Chain Reaction
MH  - Pulmonary Fibrosis/*immunology
MH  - RNA, Messenger/*biosynthesis
EDAT- 1997/02/01 00:00
MHDA- 1997/02/01 00:01
CRDT- 1997/02/01 00:00
PHST- 1997/02/01 00:00 [pubmed]
PHST- 1997/02/01 00:01 [medline]
PHST- 1997/02/01 00:00 [entrez]
PST - ppublish
SO  - Lab Invest. 1997 Feb;76(2):161-9.