ArticleDevelopmental biology2011
Kruppel-like factor 5 is required for formation and differentiation of the bladder urothelium.
Article in Developmental biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 56 citations in OpenAlex.
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- Ureter development and associated congenital anomalies.Nature reviews. Nephrology · 2025Review
- KLF5 Shapes Developing Respiratory Tubules by Inhibiting Actin Asymmetry in Epithelial Cells.American journal of respiratory cell and molecular biology · 2025Article
- PPARγ promotes urothelial remodeling during urinary tract obstruction.Experimental & molecular medicine · 2025Article
- PPARG contributes to urothelial integrity in the murine ureter by activating the expression of Shh and superficial cell-specific genes.Development (Cambridge, England) · 2025Article
- Advances in tumor microenvironment and underlying molecular mechanisms of bladder cancer: a systematic review.Discover oncology · 2024Review
- Transcription factor Tcf21 modulates urinary bladder size and differentiation.Development, growth & differentiation · 2024Article
- The urothelial gene regulatory network: understanding biology to improve bladder cancer management.Oncogene · 2024Review
- Development, regeneration and tumorigenesis of the urothelium.Development (Cambridge, England) · 2022Review
- Grainyhead-like (Grhl) Target Genes in Development and Cancer.International journal of molecular sciences · 2022Review
- A stem cell marker KLF5 regulates CCAT1 via three-dimensional genome structure in colorectal cancer cells.British journal of cancer · 2022Article
- Stage-stratified molecular profiling of non-muscle-invasive bladder cancer enhances biological, clinical, and therapeutic insight.Cell reports. Medicine · 2021Article
- Alterations of Chromatin Regulators in the Pathogenesis of Urinary Bladder Urothelial Carcinoma.Cancers · 2021Review
- Pparg signaling controls bladder cancer subtype and immune exclusion.Nature communications · 2021Article
- YAP regulates alveolar epithelial cell differentiation andiScience · 2021Article
- Tumor cell heterogeneity and its transcriptional bases in pancreatic cancer: a tale of two cell types and their many variants.The EMBO journal · 2021Review
- The roles and regulation of the KLF5 transcription factor in cancers.Cancer science · 2021Review
- KLF5 Is Activated by Gene Amplification in Gastric Cancer and Is Essential for Gastric Cell Proliferation.Cells · 2021Article
- Grainyhead-Like 3 Influences Migration and Invasion of Urothelial Carcinoma Cells.International journal of molecular sciences · 2021Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Kruppel-like transcription factor 5 (Klf5) was detected in the developing and mature murine bladder urothelium. Herein we report a critical role of KLF5 in the formation and terminal differentiation of the urothelium. The Shh(GfpCre) transgene was used to delete the Klf5(floxed) alleles from bladder epithelial cells causing prenatal hydronephrosis, hydroureter, and vesicoureteric reflux. The bladder urothelium failed to stratify and did not express terminal differentiation markers characteristic of basal, intermediate, and umbrella cells including keratins 20, 14, and 5, and the uroplakins. The effects of Klf5 deletion were unique to the developing bladder epithelium since maturation of the epithelium comprising the bladder neck and urethra was unaffected by the lack of KLF5. mRNA analysis identified reductions in Pparγ, Grhl3, Elf3, and Ovol1expression in Klf5 deficient fetal bladders supporting their participation in a transcriptional network regulating bladder urothelial differentiation. KLF5 regulated expression of the mGrhl3 promoter in transient transfection assays. The absence of urothelial Klf5 altered epithelial-mesenchymal signaling leading to the formation of an ectopic alpha smooth muscle actin positive layer of cells subjacent to the epithelium and a thinner detrusor muscle that was not attributable to disruption of SHH signaling, a known mediator of detrusor morphogenesis. Deletion of Klf5 from the developing bladder urothelium blocked epithelial cell differentiation, impaired bladder morphogenesis and function causing hydroureter and hydronephrosis at birth.
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