PMID- 14592444
OWN - NLM
STAT- MEDLINE
DCOM- 20040210
LR  - 20190612
IS  - 0006-291X (Print)
IS  - 0006-291X (Linking)
VI  - 311
IP  - 2
DP  - 2003 Nov 14
TI  - Suppressor mechanism of serum thymic factor on tumor necrosis 
      factor-alpha-induced apoptosis in the mouse pancreatic beta-cell line.
PG  - 501-5
AB  - Tumor necrosis factor-alpha (TNF-alpha) is a cytokine considered to play a key 
      role in beta-cell destruction in insulin-dependent diabetes mellitus (IDDM). 
      Serum thymic factor (Facteur thymique serique; FTS) is a nonapeptide thymus 
      hormone known to inhibit IDDM in a mouse model. In this study, the effect of 
      TNF-alpha on the murine pancreatic beta-cell line MIN6 was examined. Cell 
      shrinkage and detachment were seen in cells treated with 0-50 ng/ml TNF-alpha for 
      12h. Oligonucleosomal DNA fragmentation was determined from non-adherent cells, 
      indicating that the TNF-alpha-induced cell destruction was attributed to 
      apoptosis. Fragmented DNA was quantified by enzyme-linked immunosorbent assay to 
      measure the amount of histone-bound oligonucleosomes. FTS was treated with 
      TNF-alpha and the percentage of fragmented DNA was analyzed. The data indicate a 
      distinct reduction of fragmented DNA at a concentration of 1 ng/ml FTS. 
      Expression of TNF receptor I, inducible form of nitric oxide synthase (iNOS), 
      interleukin-1 beta-converting enzyme (ICE), Bcl-2, and nuclear factor kappa B 
      (NF-kappa B) was analyzed by reverse transcriptase-polymerase chain reaction to 
      investigate the suppressor mechanism of FTS on TNF-alpha-induced apoptosis. FTS 
      treatment suppressed the expression of iNOS and Bcl-2 mRNA in TNF-alpha-treated 
      cells. The expression of NF-kappa B mRNA in TNF-alpha-treated cells was enhanced 
      after FTS treatment, while that of ICE mRNA did not change in TNF-alpha-treated 
      cells with or without FTS treatment. These results suggest that the inhibition of 
      MIN6 cell death by FTS on TNF-alpha-induced apoptosis is caused by a negative 
      feedback mechanism involving the inhibition of iNOS induction.
FAU - Yasuda, Junko
AU  - Yasuda J
AD  - Department of Molecular Immunology, School of Agricultural and Life Sciences, 
      University of Tokyo, Bunkyo-ku, Tokyo 113-8657, Japan.
FAU - Nishioka, Wakako
AU  - Nishioka W
FAU - Sakudo, Akikazu
AU  - Sakudo A
FAU - Yama, Sachiko
AU  - Yama S
FAU - Setoguchi, Ruka
AU  - Setoguchi R
FAU - Saeki, Keiichi
AU  - Saeki K
FAU - Matsumoto, Yoshitsugu
AU  - Matsumoto Y
FAU - Awaya, Akira
AU  - Awaya A
FAU - Onodera, Takashi
AU  - Onodera T
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Biochem Biophys Res Commun
JT  - Biochemical and biophysical research communications
JID - 0372516
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 9H198D04WL (Thymic Factor, Circulating)
SB  - IM
MH  - Animals
MH  - Apoptosis/*drug effects
MH  - Cell Line
MH  - DNA Damage
MH  - Dose-Response Relationship, Drug
MH  - Drug Interactions
MH  - Islets of Langerhans/cytology/*drug effects/*metabolism
MH  - Mice
MH  - Thymic Factor, Circulating/*pharmacology
MH  - Tumor Necrosis Factor-alpha/*pharmacology
EDAT- 2003/11/01 05:00
MHDA- 2004/02/11 05:00
CRDT- 2003/11/01 05:00
PHST- 2003/11/01 05:00 [pubmed]
PHST- 2004/02/11 05:00 [medline]
PHST- 2003/11/01 05:00 [entrez]
AID - S0006291X03021053 [pii]
AID - 10.1016/j.bbrc.2003.10.025 [doi]
PST - ppublish
SO  - Biochem Biophys Res Commun. 2003 Nov 14;311(2):501-5. doi: 
      10.1016/j.bbrc.2003.10.025.