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primary bladder urothelial cells  (ATCC)


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    ATCC primary bladder urothelial cells
    A Differentially expressed genes (DEGs) in full-thickness bladder tissues from HIC patients and controls identified via RNA sequencing (|log₂FC|≥2; adjusted p < 0.05, two-sided Wald test using DESeq2). Gene Ontology (GO) ( B ) and KEGG ( C ) enrichment analyses of DEGs (two-sided hypergeometric test with FDR correction). D UMAP visualization of single-cell transcriptomic landscape of urothelium, with <t>urothelial</t> cells (UCs) identified by KRT19 and UPK1A expression. GO ( E ) and KEGG ( F ) analyses of upregulated DEGs in UCs (two-sided hypergeometric test with FDR correction). GO ( G ) and KEGG ( H ) analyses of downregulated DEGs in UCs (two-sided hypergeometric test with FDR correction). I , J Gene Set Enrichment Analysis (GSEA) of altered pathways in UCs (two-sided permutation test with 1000 permutations, with multiple testing corrected using the FDR). The exact p value for TLR signaling of UCs in panel I is 0.0009. K Expression of Toll-like receptor (TLR) subtypes in UCs from HIC bladders. mRNA ( L ) and protein ( M ) expression levels of TLR3 in isolated urothelium from control and HIC patients ( n = 7 control vs. 10 HIC; data show median (IQR); two-sided Mann–Whitney U test; ns not significant; Bar for panel M: 1 cm). N Immunostaining showing the distribution of TLR3 protein in the urothelium of patients with HIC ( n = 7 control vs. 10 HIC; one section and field per patient; Bar: 100 μm). IHC immunohistochemistry, HL Hunner lesions, U urothelium, LP lamina propria (blue line), M muscularis. Source data are provided as a Source Data file.
    Primary Bladder Urothelial Cells, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 510 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/primary+bladder+urothelial+cells/pmc12868900-347-0-4?v=ATCC
    Average 99 stars, based on 510 article reviews
    primary bladder urothelial cells - by Bioz Stars, 2026-08
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    Images

    1) Product Images from "Multi-omics analysis identifies a microbiota–bile acid–TLR signaling axis driving bladder injury in interstitial cystitis"

    Article Title: Multi-omics analysis identifies a microbiota–bile acid–TLR signaling axis driving bladder injury in interstitial cystitis

    Journal: Nature Communications

    doi: 10.1038/s41467-025-68060-1

    A Differentially expressed genes (DEGs) in full-thickness bladder tissues from HIC patients and controls identified via RNA sequencing (|log₂FC|≥2; adjusted p < 0.05, two-sided Wald test using DESeq2). Gene Ontology (GO) ( B ) and KEGG ( C ) enrichment analyses of DEGs (two-sided hypergeometric test with FDR correction). D UMAP visualization of single-cell transcriptomic landscape of urothelium, with urothelial cells (UCs) identified by KRT19 and UPK1A expression. GO ( E ) and KEGG ( F ) analyses of upregulated DEGs in UCs (two-sided hypergeometric test with FDR correction). GO ( G ) and KEGG ( H ) analyses of downregulated DEGs in UCs (two-sided hypergeometric test with FDR correction). I , J Gene Set Enrichment Analysis (GSEA) of altered pathways in UCs (two-sided permutation test with 1000 permutations, with multiple testing corrected using the FDR). The exact p value for TLR signaling of UCs in panel I is 0.0009. K Expression of Toll-like receptor (TLR) subtypes in UCs from HIC bladders. mRNA ( L ) and protein ( M ) expression levels of TLR3 in isolated urothelium from control and HIC patients ( n = 7 control vs. 10 HIC; data show median (IQR); two-sided Mann–Whitney U test; ns not significant; Bar for panel M: 1 cm). N Immunostaining showing the distribution of TLR3 protein in the urothelium of patients with HIC ( n = 7 control vs. 10 HIC; one section and field per patient; Bar: 100 μm). IHC immunohistochemistry, HL Hunner lesions, U urothelium, LP lamina propria (blue line), M muscularis. Source data are provided as a Source Data file.
    Figure Legend Snippet: A Differentially expressed genes (DEGs) in full-thickness bladder tissues from HIC patients and controls identified via RNA sequencing (|log₂FC|≥2; adjusted p < 0.05, two-sided Wald test using DESeq2). Gene Ontology (GO) ( B ) and KEGG ( C ) enrichment analyses of DEGs (two-sided hypergeometric test with FDR correction). D UMAP visualization of single-cell transcriptomic landscape of urothelium, with urothelial cells (UCs) identified by KRT19 and UPK1A expression. GO ( E ) and KEGG ( F ) analyses of upregulated DEGs in UCs (two-sided hypergeometric test with FDR correction). GO ( G ) and KEGG ( H ) analyses of downregulated DEGs in UCs (two-sided hypergeometric test with FDR correction). I , J Gene Set Enrichment Analysis (GSEA) of altered pathways in UCs (two-sided permutation test with 1000 permutations, with multiple testing corrected using the FDR). The exact p value for TLR signaling of UCs in panel I is 0.0009. K Expression of Toll-like receptor (TLR) subtypes in UCs from HIC bladders. mRNA ( L ) and protein ( M ) expression levels of TLR3 in isolated urothelium from control and HIC patients ( n = 7 control vs. 10 HIC; data show median (IQR); two-sided Mann–Whitney U test; ns not significant; Bar for panel M: 1 cm). N Immunostaining showing the distribution of TLR3 protein in the urothelium of patients with HIC ( n = 7 control vs. 10 HIC; one section and field per patient; Bar: 100 μm). IHC immunohistochemistry, HL Hunner lesions, U urothelium, LP lamina propria (blue line), M muscularis. Source data are provided as a Source Data file.

    Techniques Used: RNA Sequencing, Expressing, Isolation, Control, MANN-WHITNEY, Immunostaining, Immunohistochemistry

    A Fecal microbiota transplantation (FMT) in antibiotic-pretreated mice (Abx-mice), using stool samples from healthy controls (Group A, No. of controls = 5) and HIC patients (Group B, No. of patients = 5). B Bladder weight comparison post-FMT. C Assessment of voiding behavior in FMT-recipient mice (each mouse measured once). D Evaluation of mechanical pain threshold following FMT. Comparisons: (1) Control vs. Autoimmune cystitis (AC); (2) Control vs. Control + A; (3) Control vs. Control + B; (4) AC vs. AC + A; (5) AC vs. AC + B. E Representative histological analysis of bladder tissues after FMT (one section and field per mouse). F Quantification of urinary TCDCA and TUDCA in recipient mice. For panels ( B – F ): group sizes are n = 7 for Control + A and n = 8 for all other groups; data are presented as median (IQR); statistical analysis was performed using the Kruskal–Wallis test; ns not significant. IHC immunohistochemistry, Red arrow: urothelial thinning, detachment, and exposure, Blue line: LP lamina propria, U urothelium, M muscularis. Source data are provided as a Source Data file.
    Figure Legend Snippet: A Fecal microbiota transplantation (FMT) in antibiotic-pretreated mice (Abx-mice), using stool samples from healthy controls (Group A, No. of controls = 5) and HIC patients (Group B, No. of patients = 5). B Bladder weight comparison post-FMT. C Assessment of voiding behavior in FMT-recipient mice (each mouse measured once). D Evaluation of mechanical pain threshold following FMT. Comparisons: (1) Control vs. Autoimmune cystitis (AC); (2) Control vs. Control + A; (3) Control vs. Control + B; (4) AC vs. AC + A; (5) AC vs. AC + B. E Representative histological analysis of bladder tissues after FMT (one section and field per mouse). F Quantification of urinary TCDCA and TUDCA in recipient mice. For panels ( B – F ): group sizes are n = 7 for Control + A and n = 8 for all other groups; data are presented as median (IQR); statistical analysis was performed using the Kruskal–Wallis test; ns not significant. IHC immunohistochemistry, Red arrow: urothelial thinning, detachment, and exposure, Blue line: LP lamina propria, U urothelium, M muscularis. Source data are provided as a Source Data file.

    Techniques Used: Transplantation Assay, Comparison, Control, Immunohistochemistry

    A Experimental workflow of E. avium colonization in antibiotic-pretreated mice (Abx-mice, n = 6 per group). Created in BioRender. Chen, J. (2025) https://BioRender.com/3lccwo1 . B Increased abundance of E. avium confirmed by metagenomic sequencing ( n = 6 per group). C Evaluation of voiding behavior following E. avium transplantation ( n = 6 per group; one measurement per mouse). D Measurement of mechanical pain threshold post-transplantation ( n = 6 per group). E Representative histological analysis of bladder tissues after E. avium transplantation ( n = 6 per group; one section and field per mouse). F , G Quantification of blood and urinary bile acids using comprehensive targeted bile acid profiling ( n = 6 per group). H Cell viability of human urothelial cells (HUCs) following TCDCA or TUDCA treatment ( n = 3 independent experiments). I Expression of ZO-1, TNF-α, and TLR3 following TCDCA (200 µM) exposure ( n = 3 independent experiments). J Experimental workflow of intravesical instillation of TCDCA in rats ( n = 5 per group). Created in BioRender. Chen, J. (2025) https://BioRender.com/3lccwo1 . K Evaluation of voiding function after TCDCA instillation ( n = 5 per group; each rate measured once). L Assessment of mechanical pain threshold following TCDCA exposure ( n = 5 per group). M Representative histology of bladder tissues post-instillation ( n = 5 per group; one section per rat, one field quantified per section). For panels ( B – H , K , L ): data are presented as median (IQR). Statistical analysis was performed using the two-sided Mann–Whitney U test. IHC immunohistochemistry, Red arrow: urothelial thinning, detachment, and exposure, Blue line: LP lamina propria, U urothelium, M muscularis. Source data are provided as a Source Data file.
    Figure Legend Snippet: A Experimental workflow of E. avium colonization in antibiotic-pretreated mice (Abx-mice, n = 6 per group). Created in BioRender. Chen, J. (2025) https://BioRender.com/3lccwo1 . B Increased abundance of E. avium confirmed by metagenomic sequencing ( n = 6 per group). C Evaluation of voiding behavior following E. avium transplantation ( n = 6 per group; one measurement per mouse). D Measurement of mechanical pain threshold post-transplantation ( n = 6 per group). E Representative histological analysis of bladder tissues after E. avium transplantation ( n = 6 per group; one section and field per mouse). F , G Quantification of blood and urinary bile acids using comprehensive targeted bile acid profiling ( n = 6 per group). H Cell viability of human urothelial cells (HUCs) following TCDCA or TUDCA treatment ( n = 3 independent experiments). I Expression of ZO-1, TNF-α, and TLR3 following TCDCA (200 µM) exposure ( n = 3 independent experiments). J Experimental workflow of intravesical instillation of TCDCA in rats ( n = 5 per group). Created in BioRender. Chen, J. (2025) https://BioRender.com/3lccwo1 . K Evaluation of voiding function after TCDCA instillation ( n = 5 per group; each rate measured once). L Assessment of mechanical pain threshold following TCDCA exposure ( n = 5 per group). M Representative histology of bladder tissues post-instillation ( n = 5 per group; one section per rat, one field quantified per section). For panels ( B – H , K , L ): data are presented as median (IQR). Statistical analysis was performed using the two-sided Mann–Whitney U test. IHC immunohistochemistry, Red arrow: urothelial thinning, detachment, and exposure, Blue line: LP lamina propria, U urothelium, M muscularis. Source data are provided as a Source Data file.

    Techniques Used: Sequencing, Transplantation Assay, Expressing, MANN-WHITNEY, Immunohistochemistry

    A , B Expression of tight junction protein ZO-1 and inflammatory marker TNF-α after TLR3 intervention in TCDCA-pretreated human urothelial cells (HUCs) ( n = 3 independent experiments). C Transepithelial resistance (TER) changes following TLR3 intervention in TCDCA-pretreated HUCs ( n = 3 independent experiments). D , E Expression of ZO-1 and TNF-α after pentosan polysulfate sodium (PPS) administration in TCDCA-pretreated HUCs ( n = 3 independent experiments). F TER changes following PPS intervention in TCDCA-pretreated HUCs ( n = 3 independent experiments). G Experimental workflow showing TLR3 inhibitor and PPS administration to rats following intravesical TCDCA instillation ( n = 5 per group). Created in BioRender. Chen, J. (2025) https://BioRender.com/3lccwo1 . H Assessment of voiding function (one measurement per rat) and pain threshold after TLR3 inhibition ( n = 5 per group). I Representative histological images of bladder tissues post-TLR3 inhibition ( n = 5 per group; one section and field per rat). For panels ( B , C , E , F , H ): data are presented as median (IQR). Statistical analysis was performed using the Kruskal–Wallis test. ns not significant, IHC immunohistochemistry, Red arrow: urothelial thinning, detachment, and exposure, Blue line: LP lamina propria, U urothelium, M muscularis. Source data are provided as a Source Data file.
    Figure Legend Snippet: A , B Expression of tight junction protein ZO-1 and inflammatory marker TNF-α after TLR3 intervention in TCDCA-pretreated human urothelial cells (HUCs) ( n = 3 independent experiments). C Transepithelial resistance (TER) changes following TLR3 intervention in TCDCA-pretreated HUCs ( n = 3 independent experiments). D , E Expression of ZO-1 and TNF-α after pentosan polysulfate sodium (PPS) administration in TCDCA-pretreated HUCs ( n = 3 independent experiments). F TER changes following PPS intervention in TCDCA-pretreated HUCs ( n = 3 independent experiments). G Experimental workflow showing TLR3 inhibitor and PPS administration to rats following intravesical TCDCA instillation ( n = 5 per group). Created in BioRender. Chen, J. (2025) https://BioRender.com/3lccwo1 . H Assessment of voiding function (one measurement per rat) and pain threshold after TLR3 inhibition ( n = 5 per group). I Representative histological images of bladder tissues post-TLR3 inhibition ( n = 5 per group; one section and field per rat). For panels ( B , C , E , F , H ): data are presented as median (IQR). Statistical analysis was performed using the Kruskal–Wallis test. ns not significant, IHC immunohistochemistry, Red arrow: urothelial thinning, detachment, and exposure, Blue line: LP lamina propria, U urothelium, M muscularis. Source data are provided as a Source Data file.

    Techniques Used: Expressing, Marker, Inhibition, Immunohistochemistry



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    A Differentially expressed genes (DEGs) in full-thickness bladder tissues from HIC patients and controls identified via RNA sequencing (|log₂FC|≥2; adjusted p < 0.05, two-sided Wald test using DESeq2). Gene Ontology (GO) ( B ) and KEGG ( C ) enrichment analyses of DEGs (two-sided hypergeometric test with FDR correction). D UMAP visualization of single-cell transcriptomic landscape of urothelium, with urothelial cells (UCs) identified by KRT19 and UPK1A expression. GO ( E ) and KEGG ( F ) analyses of upregulated DEGs in UCs (two-sided hypergeometric test with FDR correction). GO ( G ) and KEGG ( H ) analyses of downregulated DEGs in UCs (two-sided hypergeometric test with FDR correction). I , J Gene Set Enrichment Analysis (GSEA) of altered pathways in UCs (two-sided permutation test with 1000 permutations, with multiple testing corrected using the FDR). The exact p value for TLR signaling of UCs in panel I is 0.0009. K Expression of Toll-like receptor (TLR) subtypes in UCs from HIC bladders. mRNA ( L ) and protein ( M ) expression levels of TLR3 in isolated urothelium from control and HIC patients ( n = 7 control vs. 10 HIC; data show median (IQR); two-sided Mann–Whitney U test; ns not significant; Bar for panel M: 1 cm). N Immunostaining showing the distribution of TLR3 protein in the urothelium of patients with HIC ( n = 7 control vs. 10 HIC; one section and field per patient; Bar: 100 μm). IHC immunohistochemistry, HL Hunner lesions, U urothelium, LP lamina propria (blue line), M muscularis. Source data are provided as a Source Data file.

    Journal: Nature Communications

    Article Title: Multi-omics analysis identifies a microbiota–bile acid–TLR signaling axis driving bladder injury in interstitial cystitis

    doi: 10.1038/s41467-025-68060-1

    Figure Lengend Snippet: A Differentially expressed genes (DEGs) in full-thickness bladder tissues from HIC patients and controls identified via RNA sequencing (|log₂FC|≥2; adjusted p < 0.05, two-sided Wald test using DESeq2). Gene Ontology (GO) ( B ) and KEGG ( C ) enrichment analyses of DEGs (two-sided hypergeometric test with FDR correction). D UMAP visualization of single-cell transcriptomic landscape of urothelium, with urothelial cells (UCs) identified by KRT19 and UPK1A expression. GO ( E ) and KEGG ( F ) analyses of upregulated DEGs in UCs (two-sided hypergeometric test with FDR correction). GO ( G ) and KEGG ( H ) analyses of downregulated DEGs in UCs (two-sided hypergeometric test with FDR correction). I , J Gene Set Enrichment Analysis (GSEA) of altered pathways in UCs (two-sided permutation test with 1000 permutations, with multiple testing corrected using the FDR). The exact p value for TLR signaling of UCs in panel I is 0.0009. K Expression of Toll-like receptor (TLR) subtypes in UCs from HIC bladders. mRNA ( L ) and protein ( M ) expression levels of TLR3 in isolated urothelium from control and HIC patients ( n = 7 control vs. 10 HIC; data show median (IQR); two-sided Mann–Whitney U test; ns not significant; Bar for panel M: 1 cm). N Immunostaining showing the distribution of TLR3 protein in the urothelium of patients with HIC ( n = 7 control vs. 10 HIC; one section and field per patient; Bar: 100 μm). IHC immunohistochemistry, HL Hunner lesions, U urothelium, LP lamina propria (blue line), M muscularis. Source data are provided as a Source Data file.

    Article Snippet: Primary bladder urothelial cells (ATCC, Cat. PCS-420-010) were cultured in bladder epithelial cell basal medium (ATCC, Cat. PCS-420-032) supplemented with bladder epithelial growth kit (ATCC, Cat. PCS-420-042) at 37 °C in a humidified atmosphere of 95% air and 5% CO 2 .

    Techniques: RNA Sequencing, Expressing, Isolation, Control, MANN-WHITNEY, Immunostaining, Immunohistochemistry

    A Fecal microbiota transplantation (FMT) in antibiotic-pretreated mice (Abx-mice), using stool samples from healthy controls (Group A, No. of controls = 5) and HIC patients (Group B, No. of patients = 5). B Bladder weight comparison post-FMT. C Assessment of voiding behavior in FMT-recipient mice (each mouse measured once). D Evaluation of mechanical pain threshold following FMT. Comparisons: (1) Control vs. Autoimmune cystitis (AC); (2) Control vs. Control + A; (3) Control vs. Control + B; (4) AC vs. AC + A; (5) AC vs. AC + B. E Representative histological analysis of bladder tissues after FMT (one section and field per mouse). F Quantification of urinary TCDCA and TUDCA in recipient mice. For panels ( B – F ): group sizes are n = 7 for Control + A and n = 8 for all other groups; data are presented as median (IQR); statistical analysis was performed using the Kruskal–Wallis test; ns not significant. IHC immunohistochemistry, Red arrow: urothelial thinning, detachment, and exposure, Blue line: LP lamina propria, U urothelium, M muscularis. Source data are provided as a Source Data file.

    Journal: Nature Communications

    Article Title: Multi-omics analysis identifies a microbiota–bile acid–TLR signaling axis driving bladder injury in interstitial cystitis

    doi: 10.1038/s41467-025-68060-1

    Figure Lengend Snippet: A Fecal microbiota transplantation (FMT) in antibiotic-pretreated mice (Abx-mice), using stool samples from healthy controls (Group A, No. of controls = 5) and HIC patients (Group B, No. of patients = 5). B Bladder weight comparison post-FMT. C Assessment of voiding behavior in FMT-recipient mice (each mouse measured once). D Evaluation of mechanical pain threshold following FMT. Comparisons: (1) Control vs. Autoimmune cystitis (AC); (2) Control vs. Control + A; (3) Control vs. Control + B; (4) AC vs. AC + A; (5) AC vs. AC + B. E Representative histological analysis of bladder tissues after FMT (one section and field per mouse). F Quantification of urinary TCDCA and TUDCA in recipient mice. For panels ( B – F ): group sizes are n = 7 for Control + A and n = 8 for all other groups; data are presented as median (IQR); statistical analysis was performed using the Kruskal–Wallis test; ns not significant. IHC immunohistochemistry, Red arrow: urothelial thinning, detachment, and exposure, Blue line: LP lamina propria, U urothelium, M muscularis. Source data are provided as a Source Data file.

    Article Snippet: Primary bladder urothelial cells (ATCC, Cat. PCS-420-010) were cultured in bladder epithelial cell basal medium (ATCC, Cat. PCS-420-032) supplemented with bladder epithelial growth kit (ATCC, Cat. PCS-420-042) at 37 °C in a humidified atmosphere of 95% air and 5% CO 2 .

    Techniques: Transplantation Assay, Comparison, Control, Immunohistochemistry

    A Experimental workflow of E. avium colonization in antibiotic-pretreated mice (Abx-mice, n = 6 per group). Created in BioRender. Chen, J. (2025) https://BioRender.com/3lccwo1 . B Increased abundance of E. avium confirmed by metagenomic sequencing ( n = 6 per group). C Evaluation of voiding behavior following E. avium transplantation ( n = 6 per group; one measurement per mouse). D Measurement of mechanical pain threshold post-transplantation ( n = 6 per group). E Representative histological analysis of bladder tissues after E. avium transplantation ( n = 6 per group; one section and field per mouse). F , G Quantification of blood and urinary bile acids using comprehensive targeted bile acid profiling ( n = 6 per group). H Cell viability of human urothelial cells (HUCs) following TCDCA or TUDCA treatment ( n = 3 independent experiments). I Expression of ZO-1, TNF-α, and TLR3 following TCDCA (200 µM) exposure ( n = 3 independent experiments). J Experimental workflow of intravesical instillation of TCDCA in rats ( n = 5 per group). Created in BioRender. Chen, J. (2025) https://BioRender.com/3lccwo1 . K Evaluation of voiding function after TCDCA instillation ( n = 5 per group; each rate measured once). L Assessment of mechanical pain threshold following TCDCA exposure ( n = 5 per group). M Representative histology of bladder tissues post-instillation ( n = 5 per group; one section per rat, one field quantified per section). For panels ( B – H , K , L ): data are presented as median (IQR). Statistical analysis was performed using the two-sided Mann–Whitney U test. IHC immunohistochemistry, Red arrow: urothelial thinning, detachment, and exposure, Blue line: LP lamina propria, U urothelium, M muscularis. Source data are provided as a Source Data file.

    Journal: Nature Communications

    Article Title: Multi-omics analysis identifies a microbiota–bile acid–TLR signaling axis driving bladder injury in interstitial cystitis

    doi: 10.1038/s41467-025-68060-1

    Figure Lengend Snippet: A Experimental workflow of E. avium colonization in antibiotic-pretreated mice (Abx-mice, n = 6 per group). Created in BioRender. Chen, J. (2025) https://BioRender.com/3lccwo1 . B Increased abundance of E. avium confirmed by metagenomic sequencing ( n = 6 per group). C Evaluation of voiding behavior following E. avium transplantation ( n = 6 per group; one measurement per mouse). D Measurement of mechanical pain threshold post-transplantation ( n = 6 per group). E Representative histological analysis of bladder tissues after E. avium transplantation ( n = 6 per group; one section and field per mouse). F , G Quantification of blood and urinary bile acids using comprehensive targeted bile acid profiling ( n = 6 per group). H Cell viability of human urothelial cells (HUCs) following TCDCA or TUDCA treatment ( n = 3 independent experiments). I Expression of ZO-1, TNF-α, and TLR3 following TCDCA (200 µM) exposure ( n = 3 independent experiments). J Experimental workflow of intravesical instillation of TCDCA in rats ( n = 5 per group). Created in BioRender. Chen, J. (2025) https://BioRender.com/3lccwo1 . K Evaluation of voiding function after TCDCA instillation ( n = 5 per group; each rate measured once). L Assessment of mechanical pain threshold following TCDCA exposure ( n = 5 per group). M Representative histology of bladder tissues post-instillation ( n = 5 per group; one section per rat, one field quantified per section). For panels ( B – H , K , L ): data are presented as median (IQR). Statistical analysis was performed using the two-sided Mann–Whitney U test. IHC immunohistochemistry, Red arrow: urothelial thinning, detachment, and exposure, Blue line: LP lamina propria, U urothelium, M muscularis. Source data are provided as a Source Data file.

    Article Snippet: Primary bladder urothelial cells (ATCC, Cat. PCS-420-010) were cultured in bladder epithelial cell basal medium (ATCC, Cat. PCS-420-032) supplemented with bladder epithelial growth kit (ATCC, Cat. PCS-420-042) at 37 °C in a humidified atmosphere of 95% air and 5% CO 2 .

    Techniques: Sequencing, Transplantation Assay, Expressing, MANN-WHITNEY, Immunohistochemistry

    A , B Expression of tight junction protein ZO-1 and inflammatory marker TNF-α after TLR3 intervention in TCDCA-pretreated human urothelial cells (HUCs) ( n = 3 independent experiments). C Transepithelial resistance (TER) changes following TLR3 intervention in TCDCA-pretreated HUCs ( n = 3 independent experiments). D , E Expression of ZO-1 and TNF-α after pentosan polysulfate sodium (PPS) administration in TCDCA-pretreated HUCs ( n = 3 independent experiments). F TER changes following PPS intervention in TCDCA-pretreated HUCs ( n = 3 independent experiments). G Experimental workflow showing TLR3 inhibitor and PPS administration to rats following intravesical TCDCA instillation ( n = 5 per group). Created in BioRender. Chen, J. (2025) https://BioRender.com/3lccwo1 . H Assessment of voiding function (one measurement per rat) and pain threshold after TLR3 inhibition ( n = 5 per group). I Representative histological images of bladder tissues post-TLR3 inhibition ( n = 5 per group; one section and field per rat). For panels ( B , C , E , F , H ): data are presented as median (IQR). Statistical analysis was performed using the Kruskal–Wallis test. ns not significant, IHC immunohistochemistry, Red arrow: urothelial thinning, detachment, and exposure, Blue line: LP lamina propria, U urothelium, M muscularis. Source data are provided as a Source Data file.

    Journal: Nature Communications

    Article Title: Multi-omics analysis identifies a microbiota–bile acid–TLR signaling axis driving bladder injury in interstitial cystitis

    doi: 10.1038/s41467-025-68060-1

    Figure Lengend Snippet: A , B Expression of tight junction protein ZO-1 and inflammatory marker TNF-α after TLR3 intervention in TCDCA-pretreated human urothelial cells (HUCs) ( n = 3 independent experiments). C Transepithelial resistance (TER) changes following TLR3 intervention in TCDCA-pretreated HUCs ( n = 3 independent experiments). D , E Expression of ZO-1 and TNF-α after pentosan polysulfate sodium (PPS) administration in TCDCA-pretreated HUCs ( n = 3 independent experiments). F TER changes following PPS intervention in TCDCA-pretreated HUCs ( n = 3 independent experiments). G Experimental workflow showing TLR3 inhibitor and PPS administration to rats following intravesical TCDCA instillation ( n = 5 per group). Created in BioRender. Chen, J. (2025) https://BioRender.com/3lccwo1 . H Assessment of voiding function (one measurement per rat) and pain threshold after TLR3 inhibition ( n = 5 per group). I Representative histological images of bladder tissues post-TLR3 inhibition ( n = 5 per group; one section and field per rat). For panels ( B , C , E , F , H ): data are presented as median (IQR). Statistical analysis was performed using the Kruskal–Wallis test. ns not significant, IHC immunohistochemistry, Red arrow: urothelial thinning, detachment, and exposure, Blue line: LP lamina propria, U urothelium, M muscularis. Source data are provided as a Source Data file.

    Article Snippet: Primary bladder urothelial cells (ATCC, Cat. PCS-420-010) were cultured in bladder epithelial cell basal medium (ATCC, Cat. PCS-420-032) supplemented with bladder epithelial growth kit (ATCC, Cat. PCS-420-042) at 37 °C in a humidified atmosphere of 95% air and 5% CO 2 .

    Techniques: Expressing, Marker, Inhibition, Immunohistochemistry

    Genotoxicity of acrolein using the γ-H2AX assay in canine urothelial cell lines K9TCC-AxC ( Panel A ; *** P = 0.0001) and K9TCC-SH ( Panel B ; * P = 0.014).

    Journal: Journal of Clinical and Translational Science

    Article Title: Urothelial genotoxicity of environmental chemicals detected in the urine of healthy dogs and their owners

    doi: 10.1017/cts.2024.546

    Figure Lengend Snippet: Genotoxicity of acrolein using the γ-H2AX assay in canine urothelial cell lines K9TCC-AxC ( Panel A ; *** P = 0.0001) and K9TCC-SH ( Panel B ; * P = 0.014).

    Article Snippet: Human primary urothelial cells were obtained from ATCC (Cat No: PCS-420-010, Donor ID 80203232).

    Techniques:

    Genotoxicity of acrolein using the CometChip assay in canine urothelial cell lines K9TCC-AxC ( Panel A ; *** P = 0.0001) and K9TCC-SH ( Panel B ; * P = 0.013; ** P = 0.009), and in primary canine urothelial cells ( Panel C ; * P = 0.02; ** P = 0.006; *** P ≤ 0.004).

    Journal: Journal of Clinical and Translational Science

    Article Title: Urothelial genotoxicity of environmental chemicals detected in the urine of healthy dogs and their owners

    doi: 10.1017/cts.2024.546

    Figure Lengend Snippet: Genotoxicity of acrolein using the CometChip assay in canine urothelial cell lines K9TCC-AxC ( Panel A ; *** P = 0.0001) and K9TCC-SH ( Panel B ; * P = 0.013; ** P = 0.009), and in primary canine urothelial cells ( Panel C ; * P = 0.02; ** P = 0.006; *** P ≤ 0.004).

    Article Snippet: Human primary urothelial cells were obtained from ATCC (Cat No: PCS-420-010, Donor ID 80203232).

    Techniques:

    Genotoxicity of acrolein using the γ-H2AX assay in human urothelial cell lines HT-1376 ( Panel A ; *** P ≤ 0.0009) and T24 ( Panel B ; ** P = 0.008).

    Journal: Journal of Clinical and Translational Science

    Article Title: Urothelial genotoxicity of environmental chemicals detected in the urine of healthy dogs and their owners

    doi: 10.1017/cts.2024.546

    Figure Lengend Snippet: Genotoxicity of acrolein using the γ-H2AX assay in human urothelial cell lines HT-1376 ( Panel A ; *** P ≤ 0.0009) and T24 ( Panel B ; ** P = 0.008).

    Article Snippet: Human primary urothelial cells were obtained from ATCC (Cat No: PCS-420-010, Donor ID 80203232).

    Techniques:

    Genotoxicity of acrolein using the CometChip assay in human urothelial cell lines HT-1376 ( Panel A ; ** P ≤ 0.005; *** P < 0.0001) and T24 ( Panel B ; ** P = 0.003; *** P < 0.0001), and in human primary urothelial cells ( Panel C ; * P = 0.007; *** P < 0.0001).

    Journal: Journal of Clinical and Translational Science

    Article Title: Urothelial genotoxicity of environmental chemicals detected in the urine of healthy dogs and their owners

    doi: 10.1017/cts.2024.546

    Figure Lengend Snippet: Genotoxicity of acrolein using the CometChip assay in human urothelial cell lines HT-1376 ( Panel A ; ** P ≤ 0.005; *** P < 0.0001) and T24 ( Panel B ; ** P = 0.003; *** P < 0.0001), and in human primary urothelial cells ( Panel C ; * P = 0.007; *** P < 0.0001).

    Article Snippet: Human primary urothelial cells were obtained from ATCC (Cat No: PCS-420-010, Donor ID 80203232).

    Techniques:

    Genotoxicity of inorganic arsenic (as sodium arsenite) using the CometChip assay in canine urothelial cell lines K9TCC-AxC ( Panel A ; *** P < 0.0001) and K9TCC-SH ( Panel B ; * P = 0.026; *** P < 0.0001), and in canine primary urothelial cells ( Panel C; * P = 0.04; *** P < 0.0001).

    Journal: Journal of Clinical and Translational Science

    Article Title: Urothelial genotoxicity of environmental chemicals detected in the urine of healthy dogs and their owners

    doi: 10.1017/cts.2024.546

    Figure Lengend Snippet: Genotoxicity of inorganic arsenic (as sodium arsenite) using the CometChip assay in canine urothelial cell lines K9TCC-AxC ( Panel A ; *** P < 0.0001) and K9TCC-SH ( Panel B ; * P = 0.026; *** P < 0.0001), and in canine primary urothelial cells ( Panel C; * P = 0.04; *** P < 0.0001).

    Article Snippet: Human primary urothelial cells were obtained from ATCC (Cat No: PCS-420-010, Donor ID 80203232).

    Techniques:

    Genotoxicity of inorganic arsenic (as sodium arsenite) using the CometChip assay in human urothelial cell lines HT-1376 ( Panel A ) and T24 ( Panel B ) *** P < 0.0001, and in human primary urothelial cells ( Panel C; * P = 0.005; ** P = 0.0006; *** P < 0.0001).

    Journal: Journal of Clinical and Translational Science

    Article Title: Urothelial genotoxicity of environmental chemicals detected in the urine of healthy dogs and their owners

    doi: 10.1017/cts.2024.546

    Figure Lengend Snippet: Genotoxicity of inorganic arsenic (as sodium arsenite) using the CometChip assay in human urothelial cell lines HT-1376 ( Panel A ) and T24 ( Panel B ) *** P < 0.0001, and in human primary urothelial cells ( Panel C; * P = 0.005; ** P = 0.0006; *** P < 0.0001).

    Article Snippet: Human primary urothelial cells were obtained from ATCC (Cat No: PCS-420-010, Donor ID 80203232).

    Techniques:

    p53 has a necessary and sufficient role in repressing MCOLN1 in both transformed and healthy urothelial cells (A) Bar graph showing relative MCOLN1 expression in the indicated bladder cancer cell lines treated with control siRNA or siRNA against TP53 (75 nM) for either 2 or 5 days. For each cell type values were normalized to HT1197 control mean. Circles represent independent biological repeats and the values shown represent mean ± SEM; ∗, p < 0.05; ∗∗, p < 0.01; ∗∗∗∗, p < 0.0001, t-tests with Bonferroni correction in case of samples used in multiple pairwise comparisons. (B) Bar graph showing relative MCOLN1 expression in the indicated bladder cancer cell lines with or without treatment with 10 μM Nutlin for 48 h. For each cell line, values were normalized to cell numbers in the untreated cohorts. Circles represent independent biological repeats and the values shown represent mean ± SEM; ∗∗∗∗, p < 0.0001,; n.s., not significant, t-tests. (C) Same as in (A) but in healthy urothelial cells. (D) Same as in (B) but in healthy urothelial cells. (E) Same as in (A) but with or without addition of TP53 siRNA ( TP53 KD) and expression of HRAS G12V as indicated below the graph. (F) Representative Western blot showing p53 and tubulin abundance in extracts generated from the cell lines indicated above the blot that were treated as indicated below the blot. (G) Quantification of the data shown in (F). Circles represent independent biological repeats and the values shown represent mean ± SEM; ∗, p < 0.05; ∗∗, p < 0.01; n.s., not significant, t-tests with Bonferroni correction in case of samples used in multiple pairwise comparisons.

    Journal: iScience

    Article Title: p53 mitigates the effects of oncogenic HRAS in urothelial cells via the repression of MCOLN1

    doi: 10.1016/j.isci.2021.102701

    Figure Lengend Snippet: p53 has a necessary and sufficient role in repressing MCOLN1 in both transformed and healthy urothelial cells (A) Bar graph showing relative MCOLN1 expression in the indicated bladder cancer cell lines treated with control siRNA or siRNA against TP53 (75 nM) for either 2 or 5 days. For each cell type values were normalized to HT1197 control mean. Circles represent independent biological repeats and the values shown represent mean ± SEM; ∗, p < 0.05; ∗∗, p < 0.01; ∗∗∗∗, p < 0.0001, t-tests with Bonferroni correction in case of samples used in multiple pairwise comparisons. (B) Bar graph showing relative MCOLN1 expression in the indicated bladder cancer cell lines with or without treatment with 10 μM Nutlin for 48 h. For each cell line, values were normalized to cell numbers in the untreated cohorts. Circles represent independent biological repeats and the values shown represent mean ± SEM; ∗∗∗∗, p < 0.0001,; n.s., not significant, t-tests. (C) Same as in (A) but in healthy urothelial cells. (D) Same as in (B) but in healthy urothelial cells. (E) Same as in (A) but with or without addition of TP53 siRNA ( TP53 KD) and expression of HRAS G12V as indicated below the graph. (F) Representative Western blot showing p53 and tubulin abundance in extracts generated from the cell lines indicated above the blot that were treated as indicated below the blot. (G) Quantification of the data shown in (F). Circles represent independent biological repeats and the values shown represent mean ± SEM; ∗, p < 0.05; ∗∗, p < 0.01; n.s., not significant, t-tests with Bonferroni correction in case of samples used in multiple pairwise comparisons.

    Article Snippet: Primary urothelial cells (ATCC PCS-420-010) Origin: Human primary urothelial cells.

    Techniques: Transformation Assay, Expressing, Control, Western Blot, Generated

    Journal: iScience

    Article Title: p53 mitigates the effects of oncogenic HRAS in urothelial cells via the repression of MCOLN1

    doi: 10.1016/j.isci.2021.102701

    Figure Lengend Snippet:

    Article Snippet: Primary urothelial cells (ATCC PCS-420-010) Origin: Human primary urothelial cells.

    Techniques: Virus, Recombinant, Transfection, Proliferation Assay, Cell Migration Assay, Reverse Transcription, SYBR Green Assay, Negative Control, Control, Sequencing, Software