PMID- 8375478
OWN - NLM
STAT- MEDLINE
DCOM- 19931021
LR  - 20141120
IS  - 0014-4827 (Print)
IS  - 0014-4827 (Linking)
VI  - 208
IP  - 2
DP  - 1993 Oct
TI  - Morphological change and destabilization of beta-actin mRNA by tumor necrosis 
      factor in human microvascular endothelial cells.
PG  - 498-503
AB  - Tumor necrosis factor-alpha (TNF-alpha) produced morphological changes from a 
      cobblestone-like shape into a spindle shape in human omental microvascular 
      endothelial (HOME) cells and also a drastic rearrangement of actin filaments. 
      Expression of beta-actin gene was diminished in HOME cells treated with TNF-alpha 
      for 24 h. Northern blot analysis of the beta-actin gene demonstrated that the 
      cellular level of beta-actin mRNA was decreased at 6-12 h after exposure to 
      TNF-alpha. However, there appeared to be no changes in cellular mRNA levels of 
      beta-tubulin, fibronectin, laminin B1, laminin B2, and laminin binding protein 
      genes after treatment with TNF-alpha. Nuclear run-on assays showed increased 
      transcription of the low-density lipoprotein receptor gene, but not of the 
      beta-actin gene. These data suggested that the TNF-alpha-induced inhibition of 
      beta-actin gene expression was not due to altered transcription activity. The 
      degradation rates of beta-actin, plasminogen activator inhibitor-1, and epidermal 
      growth factor receptor mRNAs were examined in the presence of actinomycin D. 
      beta-Actin mRNA was found to be specifically destabilized in TNF-alpha-treated 
      HOME cells, while other mRNA species were not. Coadministration of cycloheximide 
      blocked the TNF-alpha-induced degradation of beta-actin mRNA. The 
      TNF-alpha-induced destabilization of beta-actin mRNA and rearrangement of actin 
      filaments are discussed in relation to the morphological changes in human 
      microvascular endothelial cells.
FAU - Kohno, K
AU  - Kohno K
AD  - Department of Biochemistry, Oita Medical University, Japan.
FAU - Hamanaka, R
AU  - Hamanaka R
FAU - Abe, T
AU  - Abe T
FAU - Nomura, Y
AU  - Nomura Y
FAU - Morimoto, A
AU  - Morimoto A
FAU - Izumi, H
AU  - Izumi H
FAU - Shimizu, K
AU  - Shimizu K
FAU - Ono, M
AU  - Ono M
FAU - Kuwano, M
AU  - Kuwano M
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Exp Cell Res
JT  - Experimental cell research
JID - 0373226
RN  - 0 (Actins)
RN  - 0 (Cytoskeletal Proteins)
RN  - 0 (Extracellular Matrix Proteins)
RN  - 0 (RNA, Messenger)
RN  - 0 (Tumor Necrosis Factor-alpha)
SB  - IM
MH  - Actin Cytoskeleton/ultrastructure
MH  - Actins/*genetics
MH  - Cytoskeletal Proteins/genetics
MH  - Endothelium, Vascular/*metabolism
MH  - Extracellular Matrix Proteins/genetics
MH  - Gene Expression/drug effects
MH  - Humans
MH  - In Vitro Techniques
MH  - RNA, Messenger/genetics
MH  - Tumor Necrosis Factor-alpha/*pharmacology
EDAT- 1993/10/01 00:00
MHDA- 1993/10/01 00:01
CRDT- 1993/10/01 00:00
PHST- 1993/10/01 00:00 [pubmed]
PHST- 1993/10/01 00:01 [medline]
PHST- 1993/10/01 00:00 [entrez]
AID - S0014-4827(83)71272-3 [pii]
AID - 10.1006/excr.1993.1272 [doi]
PST - ppublish
SO  - Exp Cell Res. 1993 Oct;208(2):498-503. doi: 10.1006/excr.1993.1272.