ArticleThe Journal of biological chemistry2014
Slit diaphragm protein Neph1 and its signaling: a novel therapeutic target for protection of podocytes against glomerular injury.
Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 45 citations in OpenAlex.
- The Life of a Kidney Podocyte.Acta physiologica (Oxford, England) · 2025Review
- Podocyte-targeted therapies - progress and future directions.Nature reviews. Nephrology · 2024Review
- Role of the βPharmacological reports : PR · 2024Article
- An acytokinetic cell division creates PIP2-enriched membrane asymmetries leading to slit diaphragm assembly in Drosophila nephrocytes.Development (Cambridge, England) · 2023Article
- Flot2 acts as a novel mediator of podocyte injury in proteinuric kidney disease.International journal of biological sciences · 2023Article
- Zebrafish Model to Study Podocyte Function Within the Glomerular Filtration Barrier.Methods in molecular biology (Clifton, N.J.) · 2023Article
- Integrated screens uncover a cell surface tumor suppressor geneProceedings of the National Academy of Sciences of the United States of America · 2022Article
- New Insights into the Treatment of Glomerular Diseases: When Mechanisms Become Vivid.International journal of molecular sciences · 2022Review
- Cell adhesion molecule KIRREL1 is a feedback regulator of Hippo signaling recruiting SAV1 to cell-cell contact sites.Nature communications · 2022Article
- GAP-43 ameliorates Podocyte injury by decreasing nuclear NFATc1 expression.Biochemistry and biophysics reports · 2021Article
- New insight into podocyte slit diaphragm, a therapeutic target of proteinuria.Clinical and experimental nephrology · 2020Review
- The Use of High-Throughput Transcriptomics to Identify Pathways with Therapeutic Significance in Podocytes.International journal of molecular sciences · 2019Article
- Mutations in KIRREL1, a slit diaphragm component, cause steroid-resistant nephrotic syndrome.Kidney international · 2019Article
- Mitochondrial biogenesis induced by the β2-adrenergic receptor agonist formoterol accelerates podocyte recovery from glomerular injury.Kidney international · 2019Article
- Disruption of the exocyst induces podocyte loss and dysfunction.The Journal of biological chemistry · 2019Article
- A Novel CLCN5 Mutation Associated With Focal Segmental Glomerulosclerosis and Podocyte Injury.Kidney international reports · 2018Article
- Interaction of CD80 with Neph1: a potential mechanism of podocyte injury.Clinical and experimental nephrology · 2018Article
- Erzhi Formula Extracts Reverse Renal Injury in Diabetic Nephropathy Rats by Protecting the Renal Podocytes.Evidence-based complementary and alternative medicine : eCAM · 2018Article
- Myeloid-Derived Suppressor Cells Induce Podocyte Injury Through Increasing Reactive Oxygen Species in Lupus Nephritis.Frontiers in immunology · 2018Article
- Targeting Neph1 and ZO-1 protein-protein interaction in podocytes prevents podocyte injury and preserves glomerular filtration function.Scientific reports · 2017Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Podocytes are specialized epithelial cells that are critical components of the glomerular filtration barrier, and their dysfunction leads to proteinuria and renal failure. Therefore, preserving podocyte function is therapeutically significant. In this study, we identified Neph1 signaling as a therapeutic target that upon inhibition prevented podocyte damage from a glomerular injury-inducing agent puromycin aminonucleoside (PAN). To specifically inhibit Neph1 signaling, we used a protein transduction approach, where the cytoplasmic domain of Neph1 (Neph1CD) tagged with a protein transduction domain trans-activator of transcription was transduced in cultured podocytes prior to treatment with PAN. The PAN-induced Neph1 phosphorylation was significantly reduced in Neph1CD-transduced cells; in addition, these cells were resistant to PAN-induced cytoskeletal damage. The biochemical analysis using subfractionation studies showed that unlike control cells Neph1 was retained in the lipid raft fractions in the transduced cells following treatment with PAN, indicating that transduction of Neph1CD in podocytes prevented PAN-induced mislocalization of Neph1. In accordance, the immunofluorescence analysis further suggested that Neph1CD-transduced cells had increased ability to retain endogenous Neph1 at the membrane in response to PAN-induced injury. Similar results were obtained when angiotensin was used as an injury-inducing agent. Consistent with these observations, maintaining high levels of Neph1 at the membrane using a podocyte cell line overexpressing chimeric Neph1 increased the ability of podocytes to resist PAN-induced injury and PAN-induced albumin leakage. Using a zebrafish in vivo PAN and adriamycin injury models, we further demonstrated the ability of transduced Neph1CD to preserve glomerular function. Collectively, these results support the conclusion that inhibiting Neph1 signaling is therapeutically significant in preventing podocyte damage from glomerular injury.
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Registered trials
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