ArticleCell death & disease2018
Role of c-Abl and nephrin in podocyte cytoskeletal remodeling induced by angiotensin II.
Article in Cell death & disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 27 citations in OpenAlex.
- PLIN5 Protects Against Ang II-Induced Podocyte Lipotoxicity by Interacting With FKBP8 and Preserving Lipid Droplet-Mitochondria Contact.Cell proliferation · 2026Article
- Untargeted Urinary Proteomics Uncovers Nephroprotective and Systemic Adaptations after Obesity Surgery-Induced Weight Loss.Journal of proteome research · 2026Article
- Association Between Central Obesity and Membranous Nephropathy.Medical science monitor : international medical journal of experimental and clinical research · 2025Article
- Revisiting nephrin signaling and its specialized effects on the uniquely adaptable podocyte.The Biochemical journal · 2025Review
- Renin-angiotensin system-mediated nitric oxide signaling in podocytes.American journal of physiology. Renal physiology · 2024Article
- Central role of podocytes in mediating cellular cross talk in glomerular health and disease.American journal of physiology. Renal physiology · 2024Review
- Cytoskeleton Rearrangement in Podocytopathies: An Update.International journal of molecular sciences · 2024Review
- Mechanisms of inflammation modulation by different immune cells in hypertensive nephropathy.Frontiers in immunology · 2024Review
- Combination therapy with DHA and BMSCs suppressed podocyte injury and attenuated renal fibrosis by modulating the TGF-Renal failure · 2023Article
- Sirt6 deficiency contributes to mitochondrial fission and oxidative damage in podocytes via ROCK1-Drp1 signalling pathway.Cell proliferation · 2022Article
- Nitric-Oxide-Mediated Signaling in Podocyte Pathophysiology.Biomolecules · 2022Review
- Mfn2 Regulates High Glucose-Induced MAMs Dysfunction and Apoptosis in PodocytesFrontiers in cell and developmental biology · 2021Article
- Mitoquinone Protects Podocytes from Angiotensin II-Induced Mitochondrial Dysfunction and Injury via the Keap1-Nrf2 Signaling Pathway.Oxidative medicine and cellular longevity · 2021Article
- Huidouba Improved Podocyte Injury by Down-Regulating Nox4 Expression in Rats With Diabetic Nephropathy.Frontiers in pharmacology · 2020Article
- Sirt6 deficiency aggravates angiotensin II-induced cholesterol accumulation and injury in podocytes.Theranostics · 2020Article
- [Effect and molecular mechanism of interferon-α on podocyte apoptosis induced by hepatitis B virus X protein].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2019Article
- Hepatitis B virus X protein decreases nephrin expression and induces podocyte apoptosis via activating STAT3.Experimental and therapeutic medicine · 2019Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Our previous study showed that angiotensin II (Ang II) exposure diminished the interaction between nephrin and c-Abl, then c-Abl mediated SHIP2-Akt pathway in the process of podocyte injury in vivo and vitro. However, the relationship between nephrin and c-Abl was unknown. Recently, various studies showed that nephrin was required for cytoskeletal remodeling in glomerular podocytes. But its specific mechanisms remain incompletely understood. As a nonreceptor tyrosine kinase involved in cytoskeletal regulation, c-Abl may be a candidate of signaling proteins interacting with Src homology 2/3 (SH2/SH3) domains of nephrin. Therefore, it is proposed that c-Abl contributes to nephrin-dependent cytoskeletal remodeling of podocytes. Herein, we observed that nephrin-c-Abl colocalization were suppressed in glomeruli of patients with proteinuria. Next, CD16/7-nephrin and c-Abl vectors were constructed to investigate the nephrin-c-Abl signaling pathway in podocyte actin-cytoskeletal remodeling. The disorganized cytoskeleton stimulated by cytochalasin D in COS7 cells was dramatically restored by co-transfection with phosphorylated CD16/7-nephrin and c-Abl full-length constructs. Further, co-immunoprecipitation showed that phosphorylated CD16/7-nephrin interacted with wild-type c-Abl, but not with SH2/SH3-defective c-Abl. These findings suggest that phosphorylated nephrin is able to recruit c-Abl in a SH2/SH3-dependent manner and detached c-Abl from dephosphorylated nephrin contributes to cytoskeletal remodeling in podocytes.
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