ArticleThe American journal of pathology2008
Integrin alpha1beta1 regulates matrix metalloproteinases via P38 mitogen-activated protein kinase in mesangial cells: implications for Alport syndrome.
Article in The American journal of pathology, 2008. 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, 38 citations in OpenAlex.
- Genotype-Based Molecular Mechanisms in Alport Syndrome.Journal of the American Society of Nephrology : JASN · 2025Review
- Collagen formation, function and role in kidney disease.Nature reviews. Nephrology · 2025Review
- Matrix metalloproteinases in kidney homeostasis and diseases: an update.American journal of physiology. Renal physiology · 2024Review
- Dual inhibition of the endothelin and angiotensin receptor ameliorates renal and inner ear pathologies in Alport mice.The Journal of pathology · 2023Article
- Spatially Resolved Transcriptomes of Mammalian Kidneys Illustrate the Molecular Complexity and Interactions of Functional Nephron Segments.Frontiers in medicine · 2022Article
- Hearing Function, Degeneration, and Disease: Spotlight on the Stria Vascularis.Frontiers in cell and developmental biology · 2022Review
- Molecular Basis, Diagnostic Challenges and Therapeutic Approaches of Alport Syndrome: A Primer for Clinicians.International journal of molecular sciences · 2021Review
- Endothelin-1 mediated induction of extracellular matrix genes in strial marginal cells underlies strial pathology in Alport mice.Hearing research · 2016Article
- Endothelin A receptor activation on mesangial cells initiates Alport glomerular disease.Kidney international · 2016Article
- p47(phox) contributes to albuminuria and kidney fibrosis in mice.Kidney international · 2015Article
- Laminin α2-mediated focal adhesion kinase activation triggers Alport glomerular pathogenesis.PloS one · 2014Article
- α1β1 integrin/Rac1-dependent mesangial invasion of glomerular capillaries in Alport syndrome.The American journal of pathology · 2013Article
- Alport syndrome--insights from basic and clinical research.Nature reviews. Nephrology · 2013Review
- Investigating mechanisms of chronic kidney disease in mouse models.Pediatric nephrology (Berlin, Germany) · 2012Review
- Glomerular pathology in Alport syndrome: a molecular perspective.Pediatric nephrology (Berlin, Germany) · 2012Review
- Matrix metalloproteinases in kidney homeostasis and diseases.American journal of physiology. Renal physiology · 2012Review
- Collagen XIII induced in vascular endothelium mediates alpha1beta1 integrin-dependent transmigration of monocytes in renal fibrosis.The American journal of pathology · 2010Article
- Integrin alpha1beta1 regulates epidermal growth factor receptor activation by controlling peroxisome proliferator-activated receptor gamma-dependent caveolin-1 expression.Molecular and cellular biology · 2010Article
- Albumin modulates the production of matrix metalloproteinases-2 and -9 in podocytes.Journal of Huazhong University of Science and Technology. Medical sciences = Hua zhong ke ji da xue xue bao. Yi xue Ying De wen ban = Huazhong keji daxue xuebao. Yixue Yingdewen ban · 2009Article
- Biomechanical strain causes maladaptive gene regulation, contributing to Alport glomerular disease.Kidney international · 2009Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
Previous work has shown that integrin alpha1-null Alport mice exhibit attenuated glomerular disease with decreased matrix accumulation and live much longer than strain-matched Alport mice. However, the mechanism underlying this observation is unknown. Here we show that glomerular gelatinase expression, specifically matrix metalloproteinase-2 (MMP-2), MMP-9, and MMP-14, was significantly elevated in both integrin alpha1-null mice and integrin alpha1-null Alport mice relative to wild-type mice; however, only MMP-9 was elevated in glomeruli of Alport mice that express integrin alpha1. Similarly, cultured mesangial cells from alpha1-null mice showed elevated expression levels of all three MMPs, whereas mesangial cells from Alport mice show elevated expression levels of only MMP-9. In both glomeruli and cultured mesangial cells isolated from integrin alpha1-null mice, activation of the p38 and ERK branches of the mitogen-activated protein kinase pathway was also observed. The use of small molecule inhibitors demonstrated that the activation of the p38, but not ERK, pathway was linked to elevated MMP-2, -9, and -14 expression levels in mesangial cells from integrin alpha1-null mice. In contrast, elevated MMP-9 levels in mesangial cells from Alport mice were linked to ERK pathway activation. Blockade of gelatinase activity using a small molecule inhibitor (BAY-12-9566) ameliorated progression of proteinuria and restored the architecture of the glomerular basement membrane in alpha1 integrin-null Alport mice, suggesting that elevated gelatinase activity exacerbates glomerular disease progression in these mice.
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Registered trials
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