PMID- 9565575
OWN - NLM
STAT- MEDLINE
DCOM- 19980605
LR  - 20210209
IS  - 0021-9258 (Print)
IS  - 0021-9258 (Linking)
VI  - 273
IP  - 19
DP  - 1998 May 8
TI  - Autocrine regulation of macrophage differentiation and 92-kDa gelatinase 
      production by tumor necrosis factor-alpha via alpha5 beta1 integrin in HL-60 
      cells.
PG  - 11583-8
AB  - Tumor necrosis factor-alpha (TNF-alpha) gene is one of the early response genes 
      induced by phorbol 12-myristate 13-acetate (PMA) in human HL-60 myeloid leukemia 
      cells. In the present study, we examined the role of the TNF-alpha autocrine loop 
      in PMA-induced macrophage differentiation and gene expression of 92- and 72-kDa 
      gelatinases (MMP-9 and MMP-2). In HL-60 cells, PMA inhibited cell proliferation 
      and induced cell adhesion and spreading, expression of surface maturation marker 
      OKM1 and phagocytic activity, as well as the expression of both gelatinases, 
      which all characterize the macrophage phenotype. In contrast, TNF-alpha alone was 
      only effective in inhibiting cell proliferation. Blocking the endogenous 
      TNF-alpha activity with neutralizing anti-TNF-alpha antibodies abolished all 
      these PMA-induced events with the exception of MMP-2 gene expression. Since 
      fibronectin (FN)-mediated cell adhesion and spreading are prerequisite for both 
      macrophage differentiation and MMP-9 gene expression in HL-60 cells, we 
      hypothesized that TNF-alpha might be involved in modulating the expression of 
      either the FN or its integrin receptor genes. Whereas PMA substantially enhanced 
      the steady state mRNA and protein levels of both FN and alpha5 beta1 integrins, 
      TNF-alpha alone had little effect on the expression of these genes. However, 
      anti-TNF-alpha antibodies blocked PMA-induced augmentation of both alpha5 and 
      beta1 integrin gene expression without affecting the expression of the FN gene. 
      Our results suggest that TNF-alpha may regulate macrophage differentiation and 
      critical matrix-degrading activities of myeloid progenitor cells in an autocrine 
      manner by augmenting surface levels of the alpha5 beta1 integrin, thus promoting 
      interactions with the extracellular matrix, a key event for maturation and 
      migration of these cells during inflammation.
FAU - Xie, B
AU  - Xie B
AD  - Center for Mechanistic Biology and Biotechnology, Argonne National Laboratory, 
      Argonne, Illinois 60439-4833, USA.
FAU - Laouar, A
AU  - Laouar A
FAU - Huberman, E
AU  - Huberman E
LA  - eng
PT  - Journal Article
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PL  - United States
TA  - J Biol Chem
JT  - The Journal of biological chemistry
JID - 2985121R
RN  - 0 (Fibronectins)
RN  - 0 (Macrophage-1 Antigen)
RN  - 0 (RNA, Messenger)
RN  - 0 (Receptors, Fibronectin)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - EC 3.4.24.- (Collagenases)
RN  - EC 3.4.24.- (Gelatinases)
RN  - EC 3.4.24.- (Metalloendopeptidases)
RN  - EC 3.4.24.24 (Matrix Metalloproteinase 2)
RN  - EC 3.4.24.35 (Matrix Metalloproteinase 9)
RN  - NI40JAQ945 (Tetradecanoylphorbol Acetate)
SB  - IM
MH  - Autocrine Communication
MH  - Cell Adhesion/drug effects
MH  - Cell Differentiation
MH  - Cell Division/drug effects
MH  - Collagenases/*biosynthesis/genetics
MH  - Fibronectins/genetics/metabolism
MH  - Gelatinases/genetics
MH  - Gene Expression Regulation, Developmental
MH  - HL-60 Cells
MH  - Humans
MH  - Macrophage-1 Antigen/metabolism
MH  - Macrophages/*cytology/*enzymology
MH  - Matrix Metalloproteinase 2
MH  - Matrix Metalloproteinase 9
MH  - Metalloendopeptidases/genetics
MH  - Phagocytosis/drug effects
MH  - RNA, Messenger/genetics
MH  - Receptors, Fibronectin/genetics/*physiology
MH  - Tetradecanoylphorbol Acetate/pharmacology
MH  - Tumor Necrosis Factor-alpha/*physiology
EDAT- 1998/06/13 00:00
MHDA- 1998/06/13 00:01
CRDT- 1998/06/13 00:00
PHST- 1998/06/13 00:00 [pubmed]
PHST- 1998/06/13 00:01 [medline]
PHST- 1998/06/13 00:00 [entrez]
AID - S0021-9258(19)89361-4 [pii]
AID - 10.1074/jbc.273.19.11583 [doi]
PST - ppublish
SO  - J Biol Chem. 1998 May 8;273(19):11583-8. doi: 10.1074/jbc.273.19.11583.