PMID- 8587246
OWN - NLM
STAT- MEDLINE
DCOM- 19960327
LR  - 20220317
IS  - 0085-2538 (Print)
IS  - 0085-2538 (Linking)
VI  - 48
IP  - 6
DP  - 1995 Dec
TI  - Production of monocyte chemoattractant protein-1 by bovine glomerular endothelial 
      cells.
PG  - 1866-74
AB  - To explore the role of glomerular endothelial cells (GEN) in the pathogenesis of 
      glomerulonephritis, the in vitro production of monocyte chemoattractant protein-1 
      (MCP-1) by bovine GEN was determined by chemotaxis assay, and Western blot 
      analysis, and immunocytochemistry. Monocyte chemotactic activity of 
      GEN-conditioned media was detectable by a chemotaxis assay using human peripheral 
      blood monocytes. Exposure to human recombinant interleukin-1 beta (IL-1 beta) and 
      phorbol myristate acetate (PMA) significantly increased the chemotactic activity 
      of GEN-conditioned media. A checkerboard analysis showed that the response of 
      monocytes to GEN-conditioned media was truly chemotactic. Immunoadsorption with a 
      monoclonal antibody to human MCP-1 reduced the chemotactic activity of 
      GEN-conditioned media by 85%. Northern blot analysis revealed that MCP-1 mRNA was 
      constitutively expressed by GEN and that IL-1 beta and tumor necrosis 
      factor-alpha (TNF-alpha) increased MCP-1 mRNA levels in a dose- and 
      time-dependent manner. Furthermore, PMA induced an increase in MCP-1 mRNA levels, 
      whereas dibutyryl cyclic AMP and forskolin had minimal effects. Inhibition study 
      using protein kinase inhibitors revealed that MCP-1 mRNA expression induced by 
      IL-1 beta and TNF-alpha was suppressed by the tyrosine kinase inhibitor 
      genistein, not by the protein kinase C inhibitors staurosporine or H-7, or the 
      protein kinase A inhibitor H-89, suggesting an important role of tyrosine kinase 
      in the cytokine-induced MCP-1 gene expression. Dexamethasone had a small 
      inhibitory effect on constitutive MCP-1 mRNA expression, but no effect on the 
      induction by TNF-alpha. By immunoperoxidase staining and Western blot analysis 
      using an anti-MCP-1 monoclonal antibody. MCP-1 protein was detected in untreated 
      GEN and increased by exposure to TNF-alpha. These results demonstrate the 
      cytokine-induced production of MCP-1 by GEN at gene and protein levels as well as 
      bioactivity, and suggest that GEN may participate in the development of 
      glomerulonephritis through the production of MCP-1.
FAU - Kakizaki, Y
AU  - Kakizaki Y
AD  - Department of Pediatrics, Hirosaki University School of Medicine, Japan.
FAU - Waga, S
AU  - Waga S
FAU - Sugimoto, K
AU  - Sugimoto K
FAU - Tanaka, H
AU  - Tanaka H
FAU - Nukii, K
AU  - Nukii K
FAU - Takeya, M
AU  - Takeya M
FAU - Yoshimura, T
AU  - Yoshimura T
FAU - Yokoyama, M
AU  - Yokoyama M
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 (Cytokines)
RN  - 0 (RNA, Messenger)
SB  - IM
MH  - Blotting, Northern
MH  - Blotting, Western
MH  - Cell Division
MH  - Cells, Cultured
MH  - Chemokine CCL2/*biosynthesis/genetics
MH  - Cytokines/metabolism
MH  - Endothelium/metabolism/pathology
MH  - Glomerulonephritis/*metabolism/pathology
MH  - Humans
MH  - Immunohistochemistry
MH  - Kidney Glomerulus/*metabolism/pathology
MH  - RNA, Messenger/metabolism
EDAT- 1995/12/01 00:00
MHDA- 1995/12/01 00:01
CRDT- 1995/12/01 00:00
PHST- 1995/12/01 00:00 [pubmed]
PHST- 1995/12/01 00:01 [medline]
PHST- 1995/12/01 00:00 [entrez]
AID - S0085-2538(15)59257-0 [pii]
AID - 10.1038/ki.1995.485 [doi]
PST - ppublish
SO  - Kidney Int. 1995 Dec;48(6):1866-74. doi: 10.1038/ki.1995.485.