PMID- 9407497
OWN - NLM
STAT- MEDLINE
DCOM- 19980112
LR  - 20190725
IS  - 0085-2538 (Print)
IS  - 0085-2538 (Linking)
VI  - 52
IP  - 6
DP  - 1997 Dec
TI  - Lymphocyte-derived cytokines induce sequential expression of monocyte- and T 
      cell-specific chemokines in human mesangial cells.
PG  - 1521-31
AB  - Chemokines are a family of small related proteins that play an important role in 
      the selective recruitment of different leukocyte populations to the sites of 
      inflammation. Human glomerular mesangial cells are potent producers of a variety 
      of chemokines. Here we examined the kinetics of mesangial cell chemokine 
      expression with focus on the C-C or beta chemokines monocyte chemoattractant 
      protein-1 (MCP-1), regulated upon activation, normal T cell expressed and 
      secreted (RANTES), macrophage inflammatory protein-1 alpha (MIP-1 alpha), and the 
      C-X-C or alpha chemokine interleukin-8 (IL-8) in response to lymphocyte- or 
      monocyte-derived cytokines and mesangial cell growth factors. It was found that 
      interferon-gamma (IFN-gamma), a cytokine produced by TH1 lymphocytes, synergized 
      with tumor necrosis factor-alpha (TNF-alpha) in RANTES expression and with IL-1 
      beta in MCP-1 synthesis. Time course studies revealed an early peak of mRNA 
      expression of monocyte-specific MCP-1 upon activation with TNF-alpha in contrast 
      to T cell-specific RANTES, which reached the highest mRNA level after 18 hours. 
      This sequence of TNF-alpha-induced MCP-1 and RANTES expression was confirmed on 
      the protein level. As another T-lymphocyte specific chemokine, MIP-1 alpha mRNA 
      and protein was expressed only in response to TNF-alpha plus IFN-gamma with 
      kinetics similar to those of RANTES expression. Finally, unlike other mesangial 
      growth factors basic fibroblast growth factor (bFGF) induced MCP-1, RANTES, and 
      IL-8 mRNA expression, suggesting an involvement of autocrine regulation 
      mechanisms in mesangial chemokine expression.
FAU - Schwarz, M
AU  - Schwarz M
AD  - Institute of Clinical Molecular Pharmacology, Medical School, Hannover, Germany.
FAU - Radeke, H H
AU  - Radeke HH
FAU - Resch, K
AU  - Resch K
FAU - Uciechowski, P
AU  - Uciechowski P
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Kidney Int
JT  - Kidney international
JID - 0323470
RN  - 0 (Chemokine CCL2)
RN  - 0 (Chemokine CCL5)
RN  - 0 (Cytokines)
RN  - 0 (Interleukin-1)
RN  - 0 (Interleukin-8)
RN  - 0 (Platelet-Derived Growth Factor)
RN  - 0 (RNA, Messenger)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 103107-01-3 (Fibroblast Growth Factor 2)
RN  - 82115-62-6 (Interferon-gamma)
SB  - IM
MH  - Autocrine Communication/drug effects/immunology
MH  - Cells, Cultured
MH  - Chemokine CCL2/genetics
MH  - Chemokine CCL5/genetics
MH  - Cytokines/*genetics/pharmacology
MH  - Drug Synergism
MH  - Fibroblast Growth Factor 2/pharmacology
MH  - Gene Expression Regulation/drug effects/immunology
MH  - Glomerular Mesangium/*cytology/immunology/*metabolism
MH  - Humans
MH  - Interferon-gamma/pharmacology
MH  - Interleukin-1/pharmacology
MH  - Interleukin-8/genetics
MH  - Monocytes/*metabolism
MH  - Platelet-Derived Growth Factor/pharmacology
MH  - RNA, Messenger/metabolism
MH  - T-Lymphocytes/*metabolism
MH  - Tumor Necrosis Factor-alpha/pharmacology
EDAT- 1998/01/04 00:00
MHDA- 1998/01/04 00:01
CRDT- 1998/01/04 00:00
PHST- 1998/01/04 00:00 [pubmed]
PHST- 1998/01/04 00:01 [medline]
PHST- 1998/01/04 00:00 [entrez]
AID - S0085-2538(15)60322-2 [pii]
AID - 10.1038/ki.1997.482 [doi]
PST - ppublish
SO  - Kidney Int. 1997 Dec;52(6):1521-31. doi: 10.1038/ki.1997.482.