ArticleThe American journal of pathology2000
Gelatinase B (MMP-9) is not essential in the normal kidney and does not influence progression of renal disease in a mouse model of Alport syndrome.
Article in The American journal of pathology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 62 citations in OpenAlex.
- Review
- Article
- Molecular Basis, Diagnostic Challenges and Therapeutic Approaches of Alport Syndrome: A Primer for Clinicians.International journal of molecular sciences · 2021Review
- Extracellular matrix roles in cardiorenal fibrosis: Potential therapeutic targets for CVD and CKD in the elderly.Pharmacology & therapeutics · 2019Review
- Collagen IV diseases: A focus on the glomerular basement membrane in Alport syndrome.Matrix biology : journal of the International Society for Matrix Biology · 2017Review
- Searching for a treatment for Alport syndrome using mouse models.World journal of nephrology · 2014Review
- Laminin α2-mediated focal adhesion kinase activation triggers Alport glomerular pathogenesis.PloS one · 2014Article
- Article
- Hemodialysis removes uremic toxins that alter the biological actions of endothelial cells.PloS one · 2012Article
- MMP-9 gene deletion mitigates microvascular loss in a model of ischemic acute kidney injury.American journal of physiology. Renal physiology · 2011Article
- MT1-MMP-mediated basement membrane remodeling modulates renal development.Experimental cell research · 2010Article
- Regulation of Drosophila matrix metalloprotease Mmp2 is essential for wing imaginal disc:trachea association and air sac tubulogenesis.Developmental biology · 2009Article
- MMP9 limits apoptosis and stimulates branching morphogenesis during kidney development.Journal of the American Society of Nephrology : JASN · 2009Article
- Integrin alpha1beta1 regulates matrix metalloproteinases via P38 mitogen-activated protein kinase in mesangial cells: implications for Alport syndrome.The American journal of pathology · 2008Article
- Glomerular matrix metalloproteinases and their regulators in the pathogenesis of lupus nephritis.Arthritis research & therapy · 2008Review
- 17beta-Estradiol attenuates diabetic kidney disease by regulating extracellular matrix and transforming growth factor-beta protein expression and signaling.American journal of physiology. Renal physiology · 2007Article
- Stage-specific action of matrix metalloproteinases influences progressive hereditary kidney disease.PLoS medicine · 2006Article
- MT1-MMP-dependent neovessel formation within the confines of the three-dimensional extracellular matrix.The Journal of cell biology · 2004Article
- Disruption of tissue-type plasminogen activator gene in mice reduces renal interstitial fibrosis in obstructive nephropathy.The Journal of clinical investigation · 2002Article
- Quantitative trait loci influence renal disease progression in a mouse model of Alport syndrome.The American journal of pathology · 2002Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Matrix metalloproteinases are matrix degrading enzymes implicated in many biological processes, including development and inflammation. Gelatinase B (gelB; also known as MMP-9) is expressed in the kidney and is hypothesized to be involved in basement membrane remodeling and in preventing pathogenic accumulation of extracellular matrix in the kidney. Inhibition of gelB activity in metanephric organ culture disrupts branching morphogenesis of the ureteric bud, suggesting that gelB plays a role in kidney development in vivo. We studied kidneys of gelB-deficient mice to search for developmental, histological, molecular, ultrastructural, and functional defects. Surprisingly, no differences between gelB-/- and control kidneys were detected, and renal function was normal in gelB mutants. In addition, gelB-/- embryonic kidneys developed normally in organ culture. Gelatinase B-deficient mice were bred with Col4a3-/- mice, a model for Alport syndrome, to determine whether gelB influences the progression of glomerulonephritis. This is an important question, as it has been hypothesized that proteases are involved in damaging Alport glomerular basement membrane. However, the presence or absence of gelB did not affect the rate of progression of renal disease. Thus, gelB does not have a discernible role in the normal kidney and gelB is not involved in the progression of glomerulonephritis in a mouse model of Alport syndrome.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.