Nifedipine, a calcium-channel blocker, inhibits advanced glycation end-product-induced expression of monocyte chemoattractant protein-1 in human cultured mesangial cells

T. Matsui, Shoichi Yamagishi, K. Nakamura, H. Inoue, M. Takeuchi

Research output: Contribution to journalArticle

15 Citations (Scopus)

Abstract

The interaction between advanced glycation end-products (AGEs) and their receptors mediates the progressive alteration in renal architecture and loss of renal function in diabetic nephropathy. This study investigated whether nifedipine, a widely used anti-hypertensive drug, suppresses expression of monocyte chemoattractant protein-1 (MCP-1), a chemokine that mediates the recruitment of monocytes to inflammatory sites, in AGE-exposed human cultured mesangial cells. Cells were treated with 100 μg/ml AGE-bovine serum albumin (BSA) or non-glycated BSA in the presence or absence of 1 μM nifedipine or 50 nM diphenylene iodonium, an inhibitor of reduced nicotinamide-adenine dinucleotide phosphate oxidase, for 4 or 24 h. Expression of MCP-1 mRNA was measured using a semi-quantitative reverse transcription-polymerase chain reaction; MCP-1 protein production was measured using an enzyme-linked immunosorbent assay. AGEs significantly increased both MCP-1 mRNA expression and protein production in mesangial cells; this increase was blocked by both nifedipine and diphenylene iodonium. These results suggest that nifedipine could play a protective role against early diabetic nephropathy by suppressing MCP-1 overexpression via blockade of AGE signalling in mesangial cells.

Original languageEnglish
Pages (from-to)107-112
Number of pages6
JournalJournal of International Medical Research
Volume35
Issue number1
DOIs
Publication statusPublished - 2007 Jan 1
Externally publishedYes

Keywords

  • Advanced glycation end-product (AGEs)
  • Diabetic nephropathy
  • Monocyte chemoatiractant protein-1 (MCP-1)
  • Nifedipine
  • Oxidative stress

ASJC Scopus subject areas

  • Biochemistry
  • Cell Biology
  • Biochemistry, medical

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