+1 Recommend
1 collections
      • Record: found
      • Abstract: found
      • Article: not found

      A high glucose concentration stimulates the expression of monocyte chemotactic peptide 1 in human mesangial cells.

      Nephron. Physiology

      pharmacology, Cells, Cultured, Chemokine CCL2, metabolism, Diabetic Neuropathies, physiopathology, Enzyme Inhibitors, Gene Expression Regulation, drug effects, Glomerular Mesangium, Glucose, Humans, Monocytes, Naphthalenes, Protein Kinase C, antagonists & inhibitors, RNA, Messenger, Tetradecanoylphorbol Acetate

      Read this article at

          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.


          The mechanism of glomerular infiltration of monocytes remains unknown in diabetic nephropathy. We examined the effect of a high glucose concentration on monocyte chemotactic peptide 1 (MCP-1) expression in human mesangial cells (MCs) by using enzyme-linked immunosorbent assay and reverse transcription coupled with polymerase chain reaction (PCR). More than a 50% increase in the MCP-1 protein production was observed in MCs cultured in high-glucose medium (450 mg/dl) as compared to normal glucose (100 mg/dl; 1,496 +/- 75 vs. 966 +/- 15 pg/ml after 24 h, 1,910 +/- 93 vs. 1,250 +/- 55 pg/ml after 48 h). Semiquantitative PCR showed that phorbol myristate acetate (100 nM) increased the ratio of PCR products for MCP-1 to housekeeping gene glyceraldehyde-3-phosphate dehydrogenase on densitometric results at 24 h by 2.7-fold, which was prevented by calphostin C (200 nM) pretreatment. High glucose increased the ratio by 3-fold as compared to normal glucose at 24 h (0.72 +/- 0.11 vs. 0.24 +/- 0.01). This was also suppressed by calphostin C pretreatment. These findings demonstrate that high glucose can directly increase MCP-1 expression in MCs, which may contribute to monocyte infiltration in diabetic nephropathy, and this is regulated by protein kinase C.

          Related collections

          Author and article information



          Comment on this article