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Original Paper

A High Glucose Concentration Stimulates the Expression of Monocyte Chemotactic Peptide 1 in Human Mesangial Cells

Ihm C.-G.a · Park J.-K.a · Hong S.-P.a · Lee T.-W.a · Cho B.-S.b · Kim M.J.a · Cha D.-R.c · Ha H.d

Author affiliations

Departments of a Internal Medicine and b Pediatrics, College of Medicine, Kyung Hee University, Seoul, c Department of Internal Medicine, College of Medicine, Korea University, Seoul, d Department of Pharmacology, College of Medicine, Yonsei University, Seoul, Korea

Related Articles for ""

Nephron 1998;79:33–37

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Article / Publication Details

First-Page Preview
Abstract of Original Paper

Published online: April 29, 1998
Issue release date: May 1998

Number of Print Pages: 5
Number of Figures: 3
Number of Tables: 0

ISSN: 1660-8151 (Print)
eISSN: 2235-3186 (Online)

For additional information: http://www.karger.com/NEF

Abstract

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.


Article / Publication Details

First-Page Preview
Abstract of Original Paper

Published online: April 29, 1998
Issue release date: May 1998

Number of Print Pages: 5
Number of Figures: 3
Number of Tables: 0

ISSN: 1660-8151 (Print)
eISSN: 2235-3186 (Online)

For additional information: http://www.karger.com/NEF


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