ArticleJCI insight2019
C3a and suPAR drive versican V1 expression in tubular cells of focal segmental glomerulosclerosis.
Article in JCI insight, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 37 citations in OpenAlex.
- Soluble urokinase plasminogen activator receptor promotes endoplasmic reticulum stress and apoptosis susceptibility through RAGE in sepsis acute kidney injury.Molecular medicine (Cambridge, Mass.) · 2025Article
- Advances in the diagnosis of early biomarkers for acute kidney injury: a literature review.BMC nephrology · 2025Review
- Soluble urokinase plasminogen activator receptor is associated with kidney disease and its progression in sickle cell anemia.Haematologica · 2024Article
- Integrin signaling in cancer: bidirectional mechanisms and therapeutic opportunities.Cell communication and signaling : CCS · 2023Review
- CD8 T Cell-Derived Exosomal miR-186-5p Elicits Renal Inflammation via Activating Tubular TLR7/8 Signal Axis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- Sex Difference in the Association Between Serum Versican and Albuminuria in Patients with Type 2 Diabetes Mellitus.Diabetes, metabolic syndrome and obesity : targets and therapy · 2023Article
- Renal tubular gen e biomarkers identification based on immune infiltrates in focal segmental glomerulosclerosis.Renal failure · 2022Article
- Soluble Urokinase-Type Plasminogen Activator Receptor Levels as a Predictor of Kidney Replacement Therapy in Septic Patients with Acute Kidney Injury: An Observational Study.Journal of clinical medicine · 2022Article
- Deconvolution of Focal Segmental Glomerulosclerosis Pathophysiology Using Transcriptomics Techniques.Glomerular diseases · 2021Review
- Soluble Urokinase Receptor and Acute Kidney Injury.The New England journal of medicine · 2020Article
- The Complement C3a and C3a Receptor Pathway in Kidney Diseases.Frontiers in immunology · 2020Review
Corrections and comments
- Erratum issued
Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic tubulointerstitial injury impacts the prognosis of focal segmental glomerulosclerosis (FSGS). We found that the level of versican V1 was increased in tubular cells of FSGS patients. Tubular cell-derived versican V1 induced proliferation and collagen synthesis by activating the CD44/Smad3 pathway in fibroblasts. Both urine C3a and suPAR were increased and bound to the tubular cells in FSGS patients. C3a promoted the transcription of versican by activating the AKT/β-catenin pathway. C3aR knockout decreased the expression of versican in Adriamycin-treated (ADR-treated) mice. On the other hand, suPAR bound to integrin β6 and activated Rac1, which bound to SRp40 at the 5' end of exon 7 in versican pre-mRNA. This binding inhibited the 3'-end splicing of intron 6 and the base-pair interactions between intron 6 and intron 8, leading to the formation of versican V1. Cotreatment with ADR and suPAR specifically increased the level of versican V1 in tubulointerstitial tissues and caused more obvious interstitial fibrosis in mice than treatment with only ADR. Altogether, our results show that C3a and suPAR drive versican V1 expression in tubular cells by promoting transcription and splicing, respectively, and the increases in tubular cell-derived versican V1 induce interstitial fibrosis by activating fibroblasts in FSGS.
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