PMID- 12431778
OWN - NLM
STAT- MEDLINE
DCOM- 20030227
LR  - 20190610
IS  - 0006-3002 (Print)
IS  - 0006-3002 (Linking)
VI  - 1593
IP  - 1
DP  - 2002 Dec 16
TI  - TGF-beta1 inhibits multiple caspases induced by TNF-alpha in murine osteoblastic 
      MC3T3-E1 cells.
PG  - 1-8
AB  - Tumor necrosis factor alpha (TNF-alpha) is a proinflammatory cytokine that 
      induces apoptosis in a number of cell systems, including osteoblasts. 
      Transforming growth factor beta1 (TGF-beta1) is an abundant growth factor that is 
      known to stimulate bone formation. This study was designed to examine the role of 
      TGF-beta1 on TNF-alpha-induced apoptosis in murine osteoblastic MC3T3-E1 cells. 
      Total RNA was extracted from MC3T3-E1 cells treated with 20 ng/ml of TNF-alpha, 
      10 ng/ml of TGF-beta1, or combination, for 6 h. TNF-alpha exerted a variety of 
      effects on the apoptotic gene expression in osteoblasts. Ribonuclease protection 
      assays (RPA) revealed that TNF-alpha upregulated the mRNA levels of caspase-1, 
      -7, -11, -12, and FAS. Western blot analysis showed enhanced processing of 
      caspase-1, -7, -11, and -12, with the appearance of their activated enzymes 24 h 
      after TNF-alpha treatment. In addition, caspase-3-like activity was significantly 
      activated following TNF-alpha treatment. Levels of cleaved poly(ADP-ribose) 
      polymerase and FAS protein were also elevated by TNF-alpha. Finally, Hoechst 
      staining, terminal deoxynucleotidyl-transferase nick-end labeling (TUNEL) assay, 
      and oligonucleosome ELISA all indicated that TNF-alpha induced apoptosis. In 
      contrast, the addition of TGF-beta1 attenuated all of the aforementioned effects 
      of TNF-alpha. Our results demonstrate that TGF-beta1 can decrease 
      TNF-alpha-induced apoptosis in murine osteoblasts at least in part by attenuating 
      TNF-alpha-induced caspase gene expression.
CI  - Copyright 2002 Elsevier Science B.V.
FAU - Chua, Chu Chang
AU  - Chua CC
AD  - Osteoporosis Center, James H Quillen College of Medicine, East Tennessee State 
      University, and Veterans Affairs Medical Center, Box 70432, Johnson City, TN 
      37614, USA. chua.chu@med.va.gov
FAU - Chua, Balvin H L
AU  - Chua BH
FAU - Chen, Zhongyi
AU  - Chen Z
FAU - Landy, Cathy
AU  - Landy C
FAU - Hamdy, Ronald C
AU  - Hamdy RC
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PL  - Netherlands
TA  - Biochim Biophys Acta
JT  - Biochimica et biophysica acta
JID - 0217513
RN  - 0 (Fluorescent Dyes)
RN  - 0 (Receptors, Tumor Necrosis Factor)
RN  - 0 (Recombinant Proteins)
RN  - 0 (Tgfb1 protein, mouse)
RN  - 0 (Transforming Growth Factor beta)
RN  - 0 (Transforming Growth Factor beta1)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - EC 3.4.22.- (Caspases)
RN  - LHQ7J5KV9B (Bisbenzimidazole)
SB  - IM
MH  - Animals
MH  - Apoptosis/genetics
MH  - Bisbenzimidazole
MH  - Caspases/*metabolism
MH  - Enzyme-Linked Immunosorbent Assay
MH  - Fluorescent Dyes
MH  - In Situ Nick-End Labeling
MH  - Mice
MH  - Osteoblasts/*enzymology
MH  - Receptors, Tumor Necrosis Factor/metabolism
MH  - Recombinant Proteins/genetics/metabolism
MH  - Transforming Growth Factor beta/genetics/*metabolism/pharmacology
MH  - Transforming Growth Factor beta1
MH  - Tumor Necrosis Factor-alpha/genetics/*metabolism/pharmacology
EDAT- 2002/11/15 04:00
MHDA- 2003/02/28 04:00
CRDT- 2002/11/15 04:00
PHST- 2002/11/15 04:00 [pubmed]
PHST- 2003/02/28 04:00 [medline]
PHST- 2002/11/15 04:00 [entrez]
AID - S0167488902002574 [pii]
AID - 10.1016/s0167-4889(02)00257-4 [doi]
PST - ppublish
SO  - Biochim Biophys Acta. 2002 Dec 16;1593(1):1-8. doi: 
      10.1016/s0167-4889(02)00257-4.