PMID- 11124596
OWN - NLM
STAT- MEDLINE
DCOM- 20010202
LR  - 20171101
IS  - 1660-8151 (Print)
IS  - 1660-8151 (Linking)
VI  - 86
IP  - 4
DP  - 2000 Dec
TI  - C-Type natriuretic peptide inhibits proliferation and monocyte chemoattractant 
      protein-1 secretion in cultured human mesangial cells.
PG  - 467-72
AB  - BACKGROUND: Mesangial cell proliferation and matrix accumulation are hallmarks of 
      various progressive glomerular diseases. We examined whether C-type natriuretic 
      peptide (CNP) that is known to regulate the proliferation of vascular smooth 
      muscle cells could modulate these pathological processes using human glomerular 
      mesangial cells (GMCs) in culture. METHODS: Proliferation of GMCs cultured with 
      different concentrations of CNP-22 for 48 h was determined by a colorimetric 
      assay using a tetrazolium salt. Monocyte chemoattractant protein-1 (MCP-1) and 
      type IV collagen secretion into the culture media by GMCs in the presence or 
      absence of CNP-22 were evaluated by ELISA. Expression of mRNA for natriuretic 
      peptide receptor B (NPR-B), a specific receptor for CNP, was examined by reverse 
      transcription polymerase chain reaction (RT-PCR). RESULTS: CNP-22 (1-10 microM) 
      inhibited serum-induced GMC growth in a dose-dependent manner. The amount of 
      MCP-1 in the culture supernatant was increased approximately 2.4-fold by 5 
      microg/ml of lipopolysaccharide. This increase was inhibited by CNP-22 at 0.1-1 
      microM in a dose-dependent fashion. CNP-22 (10 microM) inhibited GMC type IV 
      collagen secretion stimulated by 20 ng/ml of platelet-derived growth factor. 
      Expression of NPR-B mRNA was confirmed in GMCs by RT-PCR. CONCLUSIONS: CNP 
      suppresses GMC proliferation and MCP-1 and type IV collagen secretion by GMCs. It 
      may have a therapeutic potential against human proliferative glomerular diseases, 
      especially those with the involvement of monocytes.
FAU - Osawa, H
AU  - Osawa H
AD  - Second Department of Internal Medicine, Hirosaki University School of Medicine, 
      Hirosaki, Japan. osawa@cc.hirosaki-u.ac.jp
FAU - Yamabe, H
AU  - Yamabe H
FAU - Kaizuka, M
AU  - Kaizuka M
FAU - Tamura, N
AU  - Tamura N
FAU - Tsunoda, S
AU  - Tsunoda S
FAU - Baba, Y
AU  - Baba Y
FAU - Shirato, K
AU  - Shirato K
FAU - Tateyama, F
AU  - Tateyama F
FAU - Okumura, K
AU  - Okumura K
LA  - eng
PT  - Journal Article
PL  - Switzerland
TA  - Nephron
JT  - Nephron
JID - 0331777
RN  - 0 (Chemokine CCL2)
RN  - 0 (Culture Media)
RN  - 0 (RNA, Messenger)
RN  - 127869-51-6 (Natriuretic Peptide, C-Type)
RN  - 9007-34-5 (Collagen)
RN  - EC 4.6.1.2 (Receptors, Atrial Natriuretic Factor)
SB  - IM
MH  - Cell Division/drug effects
MH  - Cells, Cultured
MH  - Chemokine CCL2/biosynthesis/genetics/*metabolism
MH  - Collagen/metabolism
MH  - Culture Media/analysis
MH  - Depression, Chemical
MH  - Glomerular Mesangium/*cytology/drug effects/*metabolism
MH  - Humans
MH  - Natriuretic Peptide, C-Type/*pharmacology
MH  - RNA, Messenger/biosynthesis
MH  - Receptors, Atrial Natriuretic Factor/genetics/metabolism
MH  - Reverse Transcriptase Polymerase Chain Reaction
EDAT- 2000/12/22 11:00
MHDA- 2001/03/03 10:01
CRDT- 2000/12/22 11:00
PHST- 2000/12/22 11:00 [pubmed]
PHST- 2001/03/03 10:01 [medline]
PHST- 2000/12/22 11:00 [entrez]
AID - 45836 [pii]
AID - 10.1159/000045836 [doi]
PST - ppublish
SO  - Nephron. 2000 Dec;86(4):467-72. doi: 10.1159/000045836.