ArticleAdvances in bioscience and biotechnology (Print)2013
Cyclophosphamide Induces an Early Wave of Acrolein-Independent Apoptosis in the Urothelium.
Article in Advances in bioscience and biotechnology (Print), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 14 citations in OpenAlex.
- Usability Evaluation of Urinary HAI-1, STMN-1 and TN-C in the Diagnosis of Bladder Cancer.Journal of clinical medicine · 2025Article
- Purine nucleoside phosphorylase inhibition is an effective approach for the treatment of chemical hemorrhagic cystitis.JCI insight · 2024Article
- Sex Differences in Immune Cell Infiltration and Hematuria in SCI-Induced Hemorrhagic Cystitis.Pathophysiology : the official journal of the International Society for Pathophysiology · 2023Article
- Specialized pro-resolution mediators in the bladder: Receptor expression and recovery of bladder function from cystitis.Experimental biology and medicine (Maywood, N.J.) · 2022Article
- Loss of Fibroblast Growth Factor Receptor 2 (FGFR2) Leads to Defective Bladder Urothelial Regeneration after Cyclophosphamide Injury.The American journal of pathology · 2021Article
- Keratinocyte Growth Factor Reduces Injury and Leads to Early Recovery from Cyclophosphamide Bladder Injury.The American journal of pathology · 2020Article
- Intravesical Administration of Xenogeneic Porcine Urothelial Cells Attenuates Cyclophosphamide-Induced Cystitis in Mice.Cell transplantation · 2019Article
- Article
- The NLRP3 Inflammasome Mediates Inflammation Produced by Bladder Outlet Obstruction.The Journal of urology · 2016Article
- Inflammasomes are important mediators of cyclophosphamide-induced bladder inflammation.American journal of physiology. Renal physiology · 2014Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
purposeHemorrhagic cystitis (HC or bladder inflammation) affects a significant number of patients undergoing cyclophosphamide (CP) chemotherapy despite treatment with 2-mercapto MATERIALS AND
methodsApoptosis in urothelium (caspase-3/7 activity and Poly (ADP-ribosyl) polymerase (PARP) cleavage) was measured following CP administration (80 mg/kg). Sodium 2-mercaptoethane sulfonate (Mesna) was used to mask acrolein's effect. An IL-1β receptor antagonist and a cell-permeable caspase-1 inhibitor were used to assess the involvement of IL-1β and caspase-1, respectively.
resultsTwo waves of apoptosis were detected following CP administration, one peaking at 2 h and a second at 48 h. The first wave was independent of acrolein. Caspase-1 was also active at 2 h and activation of caspase-3/7 was blocked by a caspase-1 inhibitor but not an IL-1β receptor antagonist suggesting the direct activation of caspase-3/7 by caspase-1 without the need for IL-1β as an intermediate.
conclusionsOur results indicate that CP initiates an early, acrolein-independent wave of apoptosis that results from direct cleavage of caspase-3/7 by caspase-1.
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