ArticleCell death & disease2019
LIM homeodomain transcription factor Isl1 affects urethral epithelium differentiation and apoptosis via Shh.
Article in Cell death & disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- MAFB-mediated CEBPA regulated human urothelium growth through Wnt/β-catenin signaling pathway.Genes & diseases · 2025Article
- EZH2 specifically regulates ISL1 during embryonic urinary tract formation.Scientific reports · 2024Article
- Tgfbr1 controls developmental plasticity between the hindlimb and external genitalia by remodeling their regulatory landscape.Nature communications · 2024Article
- Strategies for generating mouse model resources of human disease.Protein & cell · 2023Article
- Review
- A synthetic tear protein resolves dry eye through promoting corneal nerve regeneration.Cell reports · 2022Article
- Single cell transcriptomic analysis of external genitalia reveals complex and sexually dimorphic cell populations in the early genital tubercle.Developmental biology · 2021Article
- Integrative Multi-Omics Analysis Reveals Candidate Biomarkers for Oral Squamous Cell Carcinoma.Frontiers in oncology · 2021Article
- Rathke's cleft-like cysts arise from Isl1 deletion in murine pituitary progenitors.The Journal of clinical investigation · 2020Article
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Authors and funding
8 authors.
Funding
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Abstract
Urethral hypoplasia, including failure of urethral tube closure, is one of the common phenotypes observed in hereditary human disorders, the mechanism of which remains unclear. The present study was thus designed to study the expression, functions, and related mechanisms of the LIM homeobox transcription factor Isl1 throughout mouse urethral development. Results showed that Isl1 was highly expressed in urethral epithelial cells and mesenchymal cells of the genital tubercle (GT). Functional studies were carried out by utilizing the tamoxifen-inducible Isl1-knockout mouse model. Histological and morphological results indicated that Isl1 deletion caused urethral hypoplasia and inhibited maturation of the complex urethral epithelium. In addition, we show that Isl1-deleted mice failed to maintain the progenitor cell population required for renewal of urethral epithelium during tubular morphogenesis and exhibited significantly increased cell death within the urethra. Dual-Luciferase reporter assays and yeast one-hybrid assays showed that ISL1 was essential for normal urethral development by directly targeting the Shh gene. Collectively, results presented here demonstrated that Isl1 plays a crucial role in mouse urethral development, thus increasing our potential for understanding the mechanistic basis of hereditary urethral hypoplasia.
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