ArticleAmerican journal of physiology. Renal physiology2017
Urothelial proliferation and regeneration after spinal cord injury.
Article in American journal of physiology. Renal physiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 49 citations in OpenAlex.
- Article
- TRIM29 is Critical for Bladder Cancer Progression and Modulates the Tumor-Immune Niche.Research square · 2026Article
- Global trends in platelet-rich plasma research: A bibliometric review with hotspot visualization.Medicine · 2026Review
- Cyclosporine as a Novel Therapeutic Option for Eosinophilic Cystitis in a Paraplegic Dog.Case reports in veterinary medicine · 2026Article
- Development of urinary impairment after spinal cord injury courses with altered urethral serotonin signalling in the female mice.Scientific reports · 2025Article
- Translational Pitfalls in SCI Bladder Research: The Hidden Role of Urinary Drainage Techniques in the Rat Model.Biology · 2025Article
- PPARγ promotes urothelial remodeling during urinary tract obstruction.Experimental & molecular medicine · 2025Article
- Exploring the differentiation potential of adipose tissue-derived mesenchymal stromal/stem cells and progenitor buccal epithelial cells into urothelial cells.Frontiers in bioengineering and biotechnology · 2025Article
- [Application and progress of bio-derived materials in bladder regeneration and repair].Zhongguo xiu fu chong jian wai ke za zhi = Zhongguo xiufu chongjian waike zazhi = Chinese journal of reparative and reconstructive surgery · 2024Review
- Keratin 5 basal cells are temporally regulated developmental and tissue repair progenitors in bladder urothelium.American journal of physiology. Renal physiology · 2024Article
- System failure: Systemic inflammation following spinal cord injury.European journal of immunology · 2024Review
- Transcriptomics Reveals Molecular Features of the Bilateral Pelvic Nerve Injury Rat Model of Detrusor Underactivity.Biomolecules · 2023Article
- Sex Differences in Immune Cell Infiltration and Hematuria in SCI-Induced Hemorrhagic Cystitis.Pathophysiology : the official journal of the International Society for Pathophysiology · 2023Article
- Research progress of biomaterials and innovative technologies in urinary tissue engineering.Frontiers in bioengineering and biotechnology · 2023Review
- Spinal Cord Injury Causes Marked Tissue Rearrangement in the Urethra-Experimental Study in the Rat.International journal of molecular sciences · 2022Article
- Engineered human organ-specific urethra as a functional substitute.Scientific reports · 2022Article
- Implantation of adipose-derived mesenchymal stem cell sheets promotes axonal regeneration and restores bladder function after spinal cord injury.Stem cell research & therapy · 2022Article
- Urothelial progenitors in development and repair.Pediatric nephrology (Berlin, Germany) · 2022Review
- Role of ERK signaling in bladder urothelium in response to cyclophosphamide injury.Physiological reports · 2022Article
- The urothelium: a multi-faceted barrier against a harsh environment.Mucosal immunology · 2022Review
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
The basal, intermediate, and superficial cell layers of the urothelium undergo rapid and complete recovery following acute injury; however, the effects of chronic injury on urothelial regeneration have not been well defined. To address this discrepancy, we employed a mouse model to explore urothelial changes in response to spinal cord injury (SCI), a condition characterized by life-long bladder dysfunction. One day post SCI there was a focal loss of umbrella cells, which are large cells that populate the superficial cell layer and normally express uroplakins (UPKs) and KRT20, but not KRT5, KRT14, or TP63. In response to SCI, regions of urothelium devoid of umbrella cells were replaced with small superficial cells that lacked KRT20 expression and appeared to be derived in part from the underlying intermediate cell layer, including cells positive for KRT5 and TP63. We also observed KRT14-positive basal cells that extended thin cytoplasmic extensions, which terminated in the bladder lumen. Both KRT14-positive and KRT14-negative urothelial cells proliferated 1 day post SCI, and by 7 days, cells in the underlying lamina propria, detrusor, and adventitia were also dividing. At 28 days post SCI, the urothelium appeared morphologically patent, and the number of proliferative cells decreased to baseline levels; however, patches of small superficial cells were detected that coexpressed UPKs, KRT5, KRT14, and TP63, but failed to express KRT20. Thus, unlike the rapid and complete restoration of the urothelium that occurs in response to acute injuries, regions of incompletely differentiated urothelium were observed even 28 days post SCI.
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