PMID- 19460355
OWN - NLM
STAT- MEDLINE
DCOM- 20090626
LR  - 20171116
IS  - 1090-2104 (Electronic)
IS  - 0006-291X (Linking)
VI  - 385
IP  - 2
DP  - 2009 Jul 24
TI  - Nifedipine, a calcium channel blocker, inhibits advanced glycation end product 
      (AGE)-elicited mesangial cell damage by suppressing AGE receptor (RAGE) 
      expression via peroxisome proliferator-activated receptor-gamma activation.
PG  - 269-72
LID - 10.1016/j.bbrc.2009.05.061 [doi]
AB  - The interaction between advanced glycation end products (AGE) and their receptor 
      RAGE mediates the progressive alteration in renal architecture and loss of renal 
      function in diabetic nephropathy. Oxidative stress generation and inflammation 
      also play a central role in diabetic nephropathy. This study investigated whether 
      and how nifedipine, a calcium channel blocker (CCB), blocked the AGE-elicited 
      mesangial cell damage in vitro. Nifedipine, but not amlodipine, a control CCB, 
      down-regulated RAGE mRNA levels and subsequently reduced reactive oxygen species 
      (ROS) generation in AGE-exposed mesangial cells. AGE increased mRNA levels of 
      vascular cell adhesion molecule-1 (VCAM-1) and induced monocyte chemoattractant 
      protein-1 (MCP-1) production in mesangial cells, both of which were prevented by 
      the treatment with nifedipine, but not amlodipine. The beneficial effects of 
      nifedipine on AGE-exposed mesangial cells were blocked by the simultaneous 
      treatment of GW9662, an inhibitor of peroxisome proliferator-activated 
      receptor-gamma (PPAR-gamma). Although nifedipine did not affect expression levels 
      of PPAR-gamma, it increased the PPAR-gamma transcriptional activity in mesangial 
      cells. Our present study provides a unique beneficial aspect of nifedipine on 
      diabetic nephropathy; it could work as an anti-inflammatory agent against AGE by 
      suppressing RAGE expression in cultured mesangial cells via PPAR-gamma 
      activation.
FAU - Matsui, Takanori
AU  - Matsui T
AD  - Department of Pathophysiology and Therapeutics of Diabetic Vascular 
      Complications, Kurume University School of Medicine, Kurume, Japan.
FAU - Yamagishi, Sho-ichi
AU  - Yamagishi S
FAU - Takeuchi, Masayoshi
AU  - Takeuchi M
FAU - Ueda, Seiji
AU  - Ueda S
FAU - Fukami, Kei
AU  - Fukami K
FAU - Okuda, Seiya
AU  - Okuda S
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20090519
PL  - United States
TA  - Biochem Biophys Res Commun
JT  - Biochemical and biophysical research communications
JID - 0372516
RN  - 0 (2-chloro-5-nitrobenzanilide)
RN  - 0 (Anilides)
RN  - 0 (CCL2 protein, human)
RN  - 0 (Calcium Channel Blockers)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Glycation End Products, Advanced)
RN  - 0 (PPAR gamma)
RN  - 0 (Reactive Oxygen Species)
RN  - 0 (Receptor for Advanced Glycation End Products)
RN  - 0 (Receptors, Immunologic)
RN  - I9ZF7L6G2L (Nifedipine)
SB  - IM
MH  - Anilides/pharmacology
MH  - Calcium Channel Blockers/*pharmacology
MH  - Chemokine CCL2/biosynthesis
MH  - *Cytoprotection
MH  - Glycation End Products, Advanced/*metabolism
MH  - Humans
MH  - Mesangial Cells/*drug effects/metabolism
MH  - Nifedipine/*pharmacology
MH  - PPAR gamma/*agonists
MH  - Reactive Oxygen Species/metabolism
MH  - Receptor for Advanced Glycation End Products
MH  - Receptors, Immunologic/*antagonists & inhibitors
MH  - Transcription, Genetic
EDAT- 2009/05/23 09:00
MHDA- 2009/06/27 09:00
CRDT- 2009/05/23 09:00
PHST- 2009/04/29 00:00 [received]
PHST- 2009/05/14 00:00 [accepted]
PHST- 2009/05/23 09:00 [entrez]
PHST- 2009/05/23 09:00 [pubmed]
PHST- 2009/06/27 09:00 [medline]
AID - S0006-291X(09)01002-X [pii]
AID - 10.1016/j.bbrc.2009.05.061 [doi]
PST - ppublish
SO  - Biochem Biophys Res Commun. 2009 Jul 24;385(2):269-72. doi: 
      10.1016/j.bbrc.2009.05.061. Epub 2009 May 19.