ArticleThe Journal of clinical investigation2010
Loss of the BMP antagonist USAG-1 ameliorates disease in a mouse model of the progressive hereditary kidney disease Alport syndrome.
Article in The Journal of clinical investigation, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 77 citations in OpenAlex.
- Neuroblastoma suppressor of tumorigenicity 1 is associated with the severity of interstitial fibrosis and kidney function decline in IgA nephropathy.Journal of nephrology · 2023Article
- Review
- Sostdc1 Suppression in the Absence of Sclerostin Potentiates Anabolic Action of Cortical Bone in Mice.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2023Article
- Neuroblastoma suppressor of tumorigenicity 1 is a circulating protein associated with progression to end-stage kidney disease in diabetes.Science translational medicine · 2022Article
- Article
- Simultaneous stabilization of actin cytoskeleton in multiple nephron-specific cells protects the kidney from diverse injury.Nature communications · 2022Article
- Role of Sostdc1 in skeletal biology and cancer.Frontiers in physiology · 2022Review
- Molecular and Cellular Mechanisms Underlying the Initiation and Progression of Alport Glomerular Pathology.Frontiers in medicine · 2022Review
- Uterine Sensitization-Associated Gene-1 in the Progression of Kidney Diseases.Journal of immunology research · 2021Review
- Modification of an aggressive model of Alport Syndrome reveals early differences in disease pathogenesis due to genetic background.Scientific reports · 2019Article
- Sostdc1 is expressed in all major compartments of developing and adult mammalian eyes.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2019Article
- Grem2 mediates podocyte apoptosis in high glucose milieu.Biochimie · 2019Article
- Febuxostat inhibits TGF‑β1‑induced epithelial‑mesenchymal transition via downregulation of USAG‑1 expression in Madin‑Darby canine kidney cells in vitro.Molecular medicine reports · 2019Article
- A review of clinical characteristics and genetic backgrounds in Alport syndrome.Clinical and experimental nephrology · 2019Review
- Functional heterogeneity of resident fibroblasts in the kidney.Proceedings of the Japan Academy. Series B, Physical and biological sciences · 2019Review
- The activin receptor is stimulated in the skeleton, vasculature, heart, and kidney during chronic kidney disease.Kidney international · 2018Article
- Angiotensin-converting enzyme 2 amplification limited to the circulation does not protect mice from development of diabetic nephropathy.Kidney international · 2017Article
- Novel Anti-fibrotic Therapies.Frontiers in pharmacology · 2017Review
- Collagen IV diseases: A focus on the glomerular basement membrane in Alport syndrome.Matrix biology : journal of the International Society for Matrix Biology · 2017Review
- Pentraxin-2 suppresses c-Jun/AP-1 signaling to inhibit progressive fibrotic disease.JCI insight · 2016Article
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Authors and funding
20 authors at 8 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The glomerular basement membrane (GBM) is a key component of the filtering unit in the kidney. Mutations involving any of the collagen IV genes (COL4A3, COL4A4, and COL4A5) affect GBM assembly and cause Alport syndrome, a progressive hereditary kidney disease with no definitive therapy. Previously, we have demonstrated that the bone morphogenetic protein (BMP) antagonist uterine sensitization-associated gene-1 (USAG-1) negatively regulates the renoprotective action of BMP-7 in a mouse model of tubular injury during acute renal failure. Here, we investigated the role of USAG-1 in renal function in Col4a3-/- mice, which model Alport syndrome. Ablation of Usag1 in Col4a3-/- mice led to substantial attenuation of disease progression, normalization of GBM ultrastructure, preservation of renal function, and extension of life span. Immunohistochemical analysis revealed that USAG-1 and BMP-7 colocalized in the macula densa in the distal tubules, lying in direct contact with glomerular mesangial cells. Furthermore, in cultured mesangial cells, BMP-7 attenuated and USAG-1 enhanced the expression of MMP-12, a protease that may contribute to GBM degradation. These data suggest that the pathogenetic role of USAG-1 in Col4a3-/- mice might involve crosstalk between kidney tubules and the glomerulus and that inhibition of USAG-1 may be a promising therapeutic approach for the treatment of Alport syndrome.
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