PMID- 9846835
OWN - NLM
STAT- MEDLINE
DCOM- 19981217
LR  - 20190826
IS  - 0165-5728 (Print)
IS  - 0165-5728 (Linking)
VI  - 91
IP  - 1-2
DP  - 1998 Nov 2
TI  - Astrocyte expression of monocyte chemoattractant protein-1 is differentially 
      regulated by transforming growth factor beta.
PG  - 190-7
AB  - The pathophysiology of central nervous system (CNS) inflammatory disease is 
      dependent, in part, on leukocyte recruitment across the blood-brain barrier. The 
      expression of cytokines and chemokines by astrocytes may contribute to this 
      process. Astrocytes express monocyte chemoattractant protein-1 (MCP-1), an 
      activator of monocytes and a chemoattractant for monocytes and activated T cells. 
      We examined the regulation of MCP-1 expression in human fetal astrocytes 
      following cytokine treatment in the presence and absence of transforming growth 
      factor beta (TGF-beta). TGF-beta, TNFalpha and IL-1beta, but not IFNgamma, 
      induced MCP-1 mRNA and protein. TGF-beta, in cotreatment with TNFalpha caused an 
      additive increase in MCP-1 mRNA, but not protein. In combination with IFNgamma, 
      TGF-beta significantly increased MCP-1 mRNA and protein, as compared to either 
      untreated, TGF-beta- or IFNgamma-treated astrocytes. However, TGF-gamma in 
      cotreatment with IL-1beta decreased MCP-1 mRNA and protein, as compared to 
      IL-1beta alone. Treatment of astrocytes with TGF-beta prior to TNFalpha, IFNgamma 
      or IL-1beta treatment significantly increased MCP-1 expression. The kinetics of 
      cytokine expression in the CNS may differentially regulate astrocyte-derived 
      MCP-1 expression and subsequent recruitment and activation of leukocytes.
FAU - Weiss, J M
AU  - Weiss JM
AD  - Department of Pathology, Albert Einstein College of Medicine, Bronx, NY 10461, 
      USA. weiss@aecom.yu.edu
FAU - Berman, J W
AU  - Berman JW
LA  - eng
GR  - 11920/PHS HHS/United States
GR  - 5T32CA09173/CA/NCI NIH HHS/United States
GR  - MH52974/MH/NIMH NIH HHS/United States
GR  - etc.
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - Netherlands
TA  - J Neuroimmunol
JT  - Journal of neuroimmunology
JID - 8109498
RN  - 0 (Chemokine CCL2)
RN  - 0 (RNA, Messenger)
RN  - 0 (Transforming Growth Factor beta)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 82115-62-6 (Interferon-gamma)
SB  - IM
MH  - Astrocytes/*chemistry/physiology
MH  - Blotting, Northern
MH  - Brain/cytology/immunology
MH  - Chemokine CCL2/genetics/*immunology
MH  - Enzyme-Linked Immunosorbent Assay
MH  - Fetus/cytology
MH  - Flow Cytometry
MH  - Gene Expression/drug effects/immunology
MH  - Humans
MH  - Interferon-gamma/pharmacology
MH  - Monocytes/*chemistry
MH  - RNA, Messenger/analysis
MH  - Transforming Growth Factor beta/*immunology/pharmacology
MH  - Tumor Necrosis Factor-alpha/pharmacology
EDAT- 1998/12/10 03:02
MHDA- 2000/06/01 09:00
CRDT- 1998/12/10 03:02
PHST- 1998/12/10 03:02 [pubmed]
PHST- 2000/06/01 09:00 [medline]
PHST- 1998/12/10 03:02 [entrez]
AID - S0165-5728(98)00183-0 [pii]
AID - 10.1016/s0165-5728(98)00183-0 [doi]
PST - ppublish
SO  - J Neuroimmunol. 1998 Nov 2;91(1-2):190-7. doi: 10.1016/s0165-5728(98)00183-0.