Adrenomedullin reduces mesangial cell number and glomerular inflammation in experimental mesangioproliferative glomerulonephritis

Adrenomedullin reduces mesangial cell number and glomerular inflammation in experimental mesangioproliferative glomerulonephritis. Adrenomedullin (ADM) is a vasodilator peptide that is abundantly expressed in the kidney. ADM has antiproliferative effects on glomerular mesangial cells (MC) in vitro....

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Bibliographic Details
Published in:	Kidney international Vol. 68; no. 3; pp. 1086 - 1095
Main Authors:	Plank, Christian, Hartner, Andrea, Klanke, Bernd, Geissler, Bettina, Porst, Markus, Amann, Kerstin, Hilgers, Karl F., Rascher, Wolfgang, Datsch, Jörg
Format:	Journal Article
Language:	English
Published:	New York, NY Elsevier Inc 01-09-2005 Nature Publishing Elsevier Limited
Subjects:	Adrenomedullin Animals apoptosis Biological and medical sciences Body Weight Cell Count Fibrosis Glomerular Mesangium - drug effects Glomerular Mesangium - immunology Glomerular Mesangium - pathology Glomerulonephritis Glomerulonephritis, Membranoproliferative - drug therapy Glomerulonephritis, Membranoproliferative - immunology Glomerulonephritis, Membranoproliferative - pathology glomerulosclerosis Male Medical sciences mesangioproliferative glomerulonephritis Nephrology. Urinary tract diseases Nephropathies. Renovascular diseases. Renal failure Peptides - pharmacology proliferation Rats Rats, Sprague-Dawley Thy1.1 Urine Vasodilator Agents - pharmacology apoptosis adrenomedullin proliferation glomerulosclerosis mesangioproliferative glomerulonephritis Thy1.1 Kidney disease Cell proliferation Glomerulonephritis Glomerulosclerosis Nephrology Urinary system disease Mesangial cell Adrenomedullin Inflammation Proliferation Experimental study Urology Renal glomerulus Urinary system Number Cell death Apoptosis
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Summary:	Adrenomedullin reduces mesangial cell number and glomerular inflammation in experimental mesangioproliferative glomerulonephritis. Adrenomedullin (ADM) is a vasodilator peptide that is abundantly expressed in the kidney. ADM has antiproliferative effects on glomerular mesangial cells (MC) in vitro. Whether or not treatment with ADM can reduce MC proliferation in vivo [i.e., in mesangioproliferative glomerulonephritis (GN)] is unknown. We tested the hypothesis that ADM substitution reduces MC proliferation in GN. GN in rats was induced by injection of an anti-Thy-1.1 antibody. Rats received osmotic minipumps, which continuously delivered rat ADM (500 ng/hour, N = 11), or vehicle (N = 13) from day 3 to day 6 after GN induction. Rats were sacrificed 6 days after induction of GN. On kidney sections, cells staining positive for proliferating cell nuclear antigen, mesangial cells, monocytes, and apoptotic cells were counted. Parameters of inflammation and fibrosis were measured in renal cortex and sieved glomeruli by real-time polymerase chain reaction (PCR). Systolic blood pressure, diuresis, albuminuria, creatinine clearance, microaneurysm formation, and mesangial matrix expansion were not influenced by ADM infusion. However, ADM treatment significantly reduced the number of MC, showed a tendency to reduce total glomerular cell proliferation, and significantly increased apoptosis. ADM-treated GN animals showed significantly less glomerular monocyte infiltration. ADM treatment normalized transforming growth factor (TGF)-β1 mRNA expression and reduced monocyte chemoattractant protein-1 (MCP-1), osteopontin, plasminogen activator inhibitor-1 (PAI-1), collagen I, and collagen III mRNA expression significantly. Exogenous ADM infusion reduces MC number and glomerular monocyte infiltration in the state of mesangial proliferation during acute experimental mesangioproliferative GN. These findings indicate that ADM can influence the course of mesangioproliferative GN.
Bibliography:	ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23
ISSN:	0085-2538 1523-1755
DOI:	10.1111/j.1523-1755.2005.00501.x