ArticleMolecular genetics and metabolism2011
Deficient degradation of homotrimeric type I collagen, α1(I)3 glomerulopathy in oim mice.
Article in Molecular genetics and metabolism, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
9 citing papers in PubMed, 13 citations in OpenAlex.
- Trial
- The Role of GPR39 in Regulating Osteoblast Function, Bone Matrix Quality, and Gender-Specific Bone Homeostasis.Journal of cellular physiology · 2025Article
- Collagen formation, function and role in kidney disease.Nature reviews. Nephrology · 2025Review
- Collagen Biosynthesis, Processing, and Maturation in Lung Ageing.Frontiers in medicine · 2021Review
- Quantitative proteomic profiling of extracellular matrix and site-specific collagen post-translational modifications in anMatrix biology plus · 2019Article
- Structural basis of homo- and heterotrimerization of collagen I.Nature communications · 2017Article
- Transforming growth factor-β1/Smad3-independent epithelial-mesenchymal transition in type I collagen glomerulopathy.International journal of nephrology and renovascular disease · 2017Article
- Injectable Clostridium histolyticum collagenase as a potential treatment for uterine fibroids.Reproductive sciences (Thousand Oaks, Calif.) · 2014Article
- Local transplantation is an effective method for cell delivery in the osteogenesis imperfecta murine model.International orthopaedics · 2014Article
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
Abstract
Col1a2-deficient (oim) mice synthesize homotrimeric type I collagen due to nonfunctional proα2(I) collagen chains. Our previous studies revealed a postnatal, progressive type I collagen glomerulopathy in this mouse model, but the mechanism of the sclerotic collagen accumulation within the renal mesangium remains unclear. The recent demonstration of the resistance of homotrimeric type I collagen to cleavage by matrix metalloproteinases (MMPs), led us to investigate the role of MMP-resistance in the glomerulosclerosis of Col1a2-deficient mice. We measured the pre- and post-translational expression of type I collagen and MMPs in glomeruli from heterozygous and homozygous animals. Both the heterotrimeric and homotrimeric isotypes of type I collagen were equally present in whole kidneys of heterozygous mice by immunohistochemistry and biochemical analysis, but the sclerotic glomerular collagen was at least 95-98% homotrimeric, suggesting homotrimeric type I collagen is the pathogenic isotype of type I collagen in glomerular disease. Although steady-state MMP and Col1a1 mRNA levels increased with the disease progression, we found these changes to be a secondary response to the deficient clearance of MMP-resistant homotrimers. Increased renal MMP expression was not sufficient to prevent homotrimeric type I collagen accumulation.
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Registered trials
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.