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Transitional epithelium

Transitional epithelium, also known as urothelium, is a stratified epithelial tissue specialized for lining the urinary tract, distinguished by its unique ability to undergo significant stretching and recoiling to accommodate fluctuations in urine volume without sustaining damage.^[1] This tissue type is essential for the function of distensible organs, where it forms a protective barrier that maintains impermeability to urine while allowing dynamic adaptation to mechanical stress.^[2] Structurally, transitional epithelium typically comprises 5 to 7 layers of cells when the organ is relaxed, organized into three main zones: a basal layer of cuboidal cells attached to the basement membrane, an intermediate layer of 2 to 3 layers of polyhedral cells, and an apical layer of large, dome-shaped or umbrella cells that often appear binucleated.^[2] These umbrella cells feature asymmetric unit membrane plaques rich in uroplakins and tight junctions, which contribute to the tissue's barrier properties and prevent urine permeation into underlying tissues.^[2] Upon distension, such as during bladder filling, the epithelium thins to 2 to 3 layers as the superficial cells flatten, resembling stratified squamous epithelium, while the overall structure reorganizes without cell loss or injury.^[3] Histologically, it is identified by its variable cell shapes—cuboidal to rounded in relaxed states—and prominent cytoplasmic volume in surface cells, setting it apart from other stratified epithelia.^[4] Transitional epithelium is exclusively located in the urinary system, lining the renal calyces, pelvis, ureters, urinary bladder, and proximal portion of the urethra, where it interfaces with urine and must withstand periodic expansion.^[5] Its primary functions include serving as a highly impermeable barrier to protect submucosal tissues from toxic urinary solutes, facilitating the storage and expulsion of urine through stretch-induced signaling, and contributing to sensory feedback in the micturition reflex via specialized apical structures.^[2] This adaptability not only ensures mechanical resilience but also supports the epithelium's role in ion transport regulation and pathogen resistance, underscoring its critical physiological importance.^[1]

Overview

Definition and characteristics

Transitional epithelium, also known as urothelium, is a type of stratified epithelial tissue that lines the urinary tract and is specialized for accommodating volume changes through stretching. It consists of multiple layers of cells that can shift from a rounded, cuboidal shape in the relaxed state to a flattened, squamous-like appearance when distended, enabling it to function as a highly distensible protective barrier.^[6]^[4] The nomenclature "transitional" originates from this distinctive ability of the superficial cells to undergo morphological changes in response to mechanical stretch, reflecting an intermediate adaptability not seen in other epithelia. This sets it apart from simple squamous epithelium, which forms a single, non-layered sheet suited for diffusion rather than protection against distension, and from stratified squamous epithelium, which provides durability through keratinization but lacks comparable elasticity.^[4]^[7] Key inherent properties include its multilayered organization for resilience, pronounced distensibility to prevent rupture during expansion, and overarching role as a impermeable lining to shield underlying tissues.^[6]

Location in the urinary tract

Transitional epithelium, also known as urothelium, forms the inner lining of key structures within the urinary tract, including the renal calyces and pelvis, ureters, urinary bladder, and proximal urethra.^[8]^[9] It is exclusively confined to these urinary system components and absent from the distal urethra, where stratified squamous epithelium takes over.^[10]^[11] The distribution of transitional epithelium exhibits variations in thickness that correspond to the anatomical and functional differences among these organs. In the relaxed urinary bladder, it comprises up to 7 layers of cells, whereas in the ureters it typically features 3 to 5 layers, and in the renal calyces only 2 to 3 layers.^[12]^[7] These differences in layering allow the epithelium to adapt to the varying dimensions and mechanical requirements of each structure.^[2] Endoscopically, transitional epithelium appears as a smooth, pale mucosal lining that is wrinkled in the empty state but stretches to a taut, even surface upon distension.^[13] This visible adaptability underscores its role in accommodating volume fluctuations in the urinary tract. Transitional epithelium represents a specialized adaptation evolved to support urinary retention within expandable structures like the bladder.^[14]

Microscopic Structure

Cell layers and types

Transitional epithelium, also known as urothelium, exhibits a stratified organization consisting of three primary cell layers: basal, intermediate, and superficial. The basal layer comprises one to three layers of small, cuboidal or columnar cells that rest directly on the basement membrane and serve as the proliferative compartment, containing epithelial stem cells rich in tonofilaments for attachment via hemidesmosomes.^[2]^[15] These basal cells are typically mononucleated and exhibit mitotic activity, appearing basophilic in hematoxylin and eosin (H&E) staining due to their high content of ribosomes and rough endoplasmic reticulum.^[2] The intermediate layer consists of two to several layers of larger, polygonal or pear-shaped cells that are uninucleated or occasionally binucleated, with prominent Golgi apparatus involved in protein packaging and transport.^[6]^[16] These cells undergo differentiation from the basal layer and contribute to the variable thickness of the epithelium, showing moderate basophilia in H&E preparations. Some intermediate cells may exhibit polyploidy as they mature, though this is more pronounced in the superficial layer.^[17] The superficial or apical layer is formed by a single tier of large, dome-shaped umbrella cells that often cover three to four underlying cells, providing broad coverage of the surface; these cells are characteristically binucleate or multinucleate and polyploid (up to octoploid), with abundant cytoplasm that stains eosinophilic in H&E due to keratin-like filaments.^[2]^[17] Umbrella cells have diameters of approximately 50–120 μm, while basal cells measure 5–10 μm and intermediate cells ~20 μm in diameter.^[18] The total number of cell layers in transitional epithelium varies from 3 to 7 depending on the degree of distension, thinning to 2-3 layers when stretched without loss of integrity.^[2] Unlike other stratified epithelia such as keratinized squamous epithelium, transitional epithelium lacks full keratinization and does not produce a stratum corneum, instead maintaining flexibility through its unique cellular adaptations; the presence of binucleate umbrella cells is also distinctive to urothelium.^[6]^[2] This histological organization enables the epithelium to accommodate volume changes while preserving its structure.

Apical specializations and barrier properties

The apical membrane of superficial urothelial cells, also known as umbrella cells, is highly specialized as an asymmetric unit membrane (AUM) characterized by a thicker outer leaflet compared to the inner leaflet, which enhances its barrier function.^[19] This membrane is predominantly covered (approximately 90%) by rigid, hexagonal plaques composed of uroplakins (UPs Ia, Ib, II, and IIIa), which form paracrystalline arrays of 16-nm particles visible under electron microscopy.^[20] These uroplaques are fused to the underlying cytoskeleton via interactions with actin filaments and other proteins, providing structural stability and contributing to the membrane's impermeability to water, ions, and toxins.^[21] Tight junctions in the urothelium form a complex network that seals intercellular spaces, primarily involving claudins (such as claudin-3, -4, -8, and -12) and occludin, which are enriched in the superficial cell layer to prevent paracellular leakage.^[22] Claudin-3, in particular, localizes to the terminal tight junctions of umbrella cells, reinforcing the barrier's tightness.^[23] Adjacent to these junctions, subapical fusiform vesicles—discoid structures storing reserve membrane—facilitate dynamic recycling, allowing membrane insertion or retrieval during bladder distension without compromising integrity.^[24] Key barrier components include a superficial glycosaminoglycan (GAG) layer, composed of sulfated mucopolysaccharides like chondroitin sulfate and heparan sulfate, which overlays the apical surface and repels urine solutes through its hydrophilic properties.^[25] Lipid rafts within the AUM further enhance selectivity by organizing membrane proteins and lipids into ordered domains that resist permeation.^[26] Collectively, these features yield exceptionally high transepithelial electrical resistance (TER) values exceeding 10,000 Ω·cm², far surpassing most epithelia and enabling resistance to urea, ions, and urinary toxins.^[27] Electron microscopy reveals fusiform vesicles as flattened, biconvex organelles (50-120 nm thick) packed with uroplakin plaques, serving as intracellular reservoirs for rapid membrane expansion.^[28] In the relaxed state, the apical surface displays prominent microridges—thin, finger-like projections (10-20 nm high) between plaques—that increase surface area and stabilize the membrane against mechanical stress.^[29]

Physiological Functions

Accommodation to distension

Transitional epithelium, also known as urothelium, exhibits remarkable adaptability to mechanical stress during bladder filling, transitioning from a relaxed state with 5-7 layers of cuboidal-like cells to a distended state resembling 2-3 layers of squamous-like cells. In the relaxed configuration, the superficial umbrella cells are dome-shaped, while distension causes these cells to flatten dramatically, reducing overall tissue thickness and allowing the bladder to expand without structural compromise. This process involves the coordinated sliding of intermediate cell layers and the unfolding of excess membrane stored in subapical discoidal and fusiform vesicles (DFVs) within umbrella cells, which fuse with the apical membrane via exocytosis to increase surface area.^[30] The biomechanical properties of transitional epithelium enable it to withstand significant deformation, with a reported tangent elastic modulus ranging from 2 to 6 kPa, providing the necessary resilience for bladder volume accommodation. During filling, the epithelium facilitates a 4- to 5-fold increase in bladder volume through uroplakin rearrangement in apical plaques and sliding of intermediate filaments, such as cytokeratins, which distribute mechanical forces across the tissue without causing tears. These adaptations ensure that the urothelium maintains tissue integrity under cyclic stretching, preventing leakage or damage to underlying structures.^[31]^[30] At the cellular level, binucleate umbrella cells play a central role in this accommodation, expanding their apical surface area by up to 50% or more through DFV-mediated exocytosis, which is regulated by RAB proteins including RAB8a, RAB11a, and RAB27b. These polyploid cells, often multinucleated, can increase in diameter from approximately 30-50 μm to 50-150 μm during distension, effectively covering a larger luminal area. Aquaporins such as AQP2 and AQP3, primarily localized to the basolateral membrane, contribute to water permeability, though the apical barrier limits overall flux during stretch, prioritizing mechanical expansion over osmotic adjustments.^[32]^[33]^[30] Experimental studies have validated these mechanisms using in vitro models, such as rabbit urothelium in Ussing chambers and human urothelial cultures, demonstrating tolerance to up to 200% strain without rupture while preserving barrier function through vesicle fusion and cytoskeletal reorganization. Early histological observations from the late 19th century further documented bladder distension effects on epithelial morphology, highlighting the tissue's inherent elasticity in response to volume changes.^[32]^[30]

Impermeability and sensory roles

The transitional epithelium, or urothelium, serves as a highly impermeable barrier that prevents the back-diffusion of urine solutes into the underlying tissues, maintaining blood homeostasis despite exposure to hyperosmotic and potentially toxic urinary contents. Recent studies (2025) have demonstrated that the urothelium can absorb and expel water in response to osmotic gradients, suggesting a role in modulating urine composition beyond passive barrier function.^[34] This impermeability is primarily achieved through a combination of the apical glycosaminoglycan (GAG) layer, which repels ions and hydrophilic molecules via its negatively charged sulfated polysaccharides, and tight junctions that seal the paracellular pathway between umbrella cells. For instance, the permeability coefficient for urea across the urothelium is typically less than 10^{-6} cm/s, significantly lower than in other epithelia, ensuring minimal leakage even under varying urinary concentrations.^[35]^[36]^[37] In addition to its barrier role, the urothelium contributes to sensory signaling by releasing key mediators in response to mechanical stretch or chemical irritants, thereby modulating afferent nerve activity and bladder sensation. Urothelial cells release adenosine triphosphate (ATP), nitric oxide (NO), and prostaglandins, which act on purinergic receptors (such as P2X3 on suburothelial afferent nerves) to transmit signals for voiding reflexes and pain perception. During bladder distension, ATP release increases approximately fivefold, amplifying sensory transduction without directly involving neuronal mechanisms.^[38]^[39]^[40] The urothelium also performs pH sensing through expression of acid-sensitive ion channels like TRPV1, allowing detection of urinary pH fluctuations and subsequent release of signaling molecules to protect against irritation. Furthermore, it secretes antimicrobial peptides such as beta-defensin 1, which exhibit broad-spectrum activity against uropathogens by disrupting microbial membranes, contributing to innate defense in the urinary tract. Urothelium-derived prostanoids, including prostaglandins, interact with bladder smooth muscle to enhance detrusor contractility, as demonstrated in recent studies showing stretch-induced release that potentiates voiding efficiency.^[41]^[42]^[43]

Clinical and Pathological Aspects

Urothelial carcinoma

Urothelial carcinoma (UC), previously termed transitional cell carcinoma, represents the predominant histological subtype of bladder cancer, comprising over 90% of all cases in industrialized nations. It accounts for approximately 5-10% of all urothelial carcinomas, primarily affecting the renal pelvis and ureters in the upper urinary tract.^[44] In the United States, the age-adjusted incidence rate stands at approximately 18 per 100,000 individuals annually, with an estimated 84,870 new diagnoses projected for 2025. This cancer arises from the transitional epithelium lining the urinary tract and exhibits a male predominance, typically manifesting in individuals over 65 years of age. Key risk factors for UC include tobacco smoking, which is responsible for roughly 50% of cases due to carcinogenic compounds like polycyclic aromatic hydrocarbons and aromatic amines absorbed through the lungs and excreted in urine. Occupational exposures to aromatic amines, such as those encountered in the dye, rubber, and chemical industries, further elevate risk by up to fourfold. In endemic regions, chronic infection with Schistosoma haematobium promotes squamous metaplasia and chronic inflammation, increasing UC incidence by 3- to 5-fold. Genetically, low-grade UC frequently harbors activating mutations in FGFR3, occurring in about 70% of non-muscle-invasive cases and driving papillary tumor growth. In contrast, high-grade tumors commonly feature inactivating TP53 mutations in up to 50% of instances, correlating with aggressive progression and genomic instability. UC is classified by growth pattern and invasion depth: papillary tumors form finger-like projections and constitute most non-muscle-invasive bladder cancers (NMIBC), while flat lesions include carcinoma in situ (CIS), a high-grade intraepithelial neoplasia confined to the mucosa. Approximately 70% of newly diagnosed cases are NMIBC (stages Ta or T1, limited to the epithelium or lamina propria), amenable to transurethral resection, whereas 30% present as muscle-invasive (stage T2 or higher), often requiring more aggressive intervention. CIS, detected in 1-4% of cases at diagnosis but up to 50% in high-risk NMIBC, portends a high risk of progression to invasion if untreated. Management of NMIBC centers on transurethral resection followed by intravesical Bacillus Calmette-Guérin (BCG) immunotherapy, which reduces recurrence by 30-40% and progression by 27% in intermediate- and high-risk patients. For muscle-invasive or metastatic UC, neoadjuvant chemotherapy with methotrexate, vinblastine, doxorubicin, and cisplatin (MVAC) improves survival by 5-8% when combined with radical cystectomy. In cisplatin-ineligible patients, the 2023 FDA accelerated approval of pembrolizumab monotherapy, based on the KEYNOTE-045 trial showing a 7-month overall survival benefit, has expanded first-line options. A landmark 2023 FDA approval (converted to full in December) of enfortumab vedotin, an antibody-drug conjugate targeting Nectin-4, in combination with pembrolizumab for advanced UC, demonstrated a median overall survival of 31.5 months versus 16.1 months with chemotherapy alone in the EV-302/KEYNOTE-A39 trial, marking a significant 2024 advance in systemic therapy. Five-year relative survival rates are 72% for localized disease but drop to 5% for distant metastatic UC. Emerging research highlights bladder cancer stem cells (BCSCs), a subpopulation driving recurrence and therapy resistance, with CD44+ cells identified as key targets for inhibiting self-renewal and metastasis in preclinical models. A 2025 review in iScience emphasizes therapeutic strategies against BCSCs, including CD44 blockade to enhance chemotherapy efficacy. Additionally, patient-derived organoid models of UC have advanced drug screening by recapitulating tumor heterogeneity and predicting clinical responses, as demonstrated in 2025 bioRxiv studies establishing canine urothelial organoid repositories for high-throughput testing of novel agents.

Non-malignant conditions

Interstitial cystitis/bladder pain syndrome (IC/BPS) is a chronic inflammatory condition primarily affecting the transitional epithelium of the bladder, characterized by pelvic pain, urinary urgency, and frequency without identifiable infection or other clear etiology.^[45] The disorder leads to increased urothelial permeability, often due to loss of the glycosaminoglycan (GAG) layer that normally protects the epithelium from urinary irritants, resulting in epithelial dysfunction and sensory nerve irritation.^[46] Prevalence estimates indicate that IC/BPS affects approximately 2.7% to 6.5% of women in the United States, with symptoms typically emerging in middle age.^[47] A subset of patients, around 5-10%, exhibit Hunner's lesions—distinct inflammatory areas on the bladder mucosa that represent epithelial denudation and submucosal inflammation, visible during cystoscopy.^[48] Non-malignant urothelial lesions, such as metaplasia and dysplasia, can alter the transitional epithelium without invasive growth. Squamous or intestinal metaplasia involves replacement of normal urothelial cells with keratinizing squamous or glandular cells, often in response to chronic irritation, and is generally benign though it may harbor low-grade dysplastic changes.^[49] Urothelial dysplasia, a flat pre-malignant but non-invasive lesion, features cytologic atypia within the epithelium and is considered a precursor state, though progression to malignancy is infrequent without additional factors.^[50] Radiation cystitis, a complication of pelvic radiotherapy, causes acute or chronic inflammation with denudation of umbrella cells, leading to barrier breakdown, edema, and hemorrhage in the transitional epithelium.^[51]^[52] Urinary tract infections, particularly those caused by uropathogenic Escherichia coli (UPEC), can persist in the transitional epithelium through mechanisms involving dormant intracellular bacterial reservoirs that cycle and reseed the bladder surface. A 2025 study using human urothelial organoids demonstrated how cell wall-deficient UPEC in urine facilitates recurrent infections by evading antibiotics and reattaching to the epithelium.^[53] Overactive bladder (OAB), a functional disorder, involves urothelial ATP dysregulation, where abnormal release of ATP from stretched or irritated epithelial cells hypersensitizes suburothelial afferents, contributing to detrusor overactivity and urgency.^[54] Other non-malignant conditions include chemical cystitis, such as that induced by cyclophosphamide, where metabolites like acrolein directly damage the transitional epithelium, causing edema, ulceration, and hemorrhage.^[55] Bladder stones can lead to mechanical erosion of the urothelium through chronic irritation and friction, resulting in mucosal denudation and secondary inflammation.^[56] Recent 2025 advances in OAB management target urothelial signaling pathways, including intravesical botulinum toxin A injections to modulate ATP release and afferent sensitivity, offering improved symptom control for refractory cases.^[57] Diagnosis of these conditions often relies on cystoscopy, which reveals Hunner's ulcers as erythematous, friable lesions in IC/BPS, sometimes accompanied by glomerulations after hydrodistention.^[58] Bladder biopsies are recommended to confirm pathology and exclude other conditions, particularly in cases with Hunner's lesions.^[59]

Development and Regeneration

Embryological development

The transitional epithelium, also known as urothelium, originates from distinct embryological sources depending on its location in the urinary tract. The urothelium lining the bladder derives from the endodermal epithelium of the cloaca, which differentiates into the urogenital sinus following subdivision by the urorectal septum between weeks 4 and 7 of gestation.^[60] In contrast, the urothelium of the ureters arises from the intermediate mesoderm through outgrowth of the ureteric bud, which branches from the mesonephric duct around week 5.^[61] This dual origin reflects the integrated development of the urogenital system, with the cloacal membrane rupturing shortly after division to establish separate anal and urogenital openings by approximately week 7.^[60] Differentiation of the urothelium begins around week 7, as the primitive epithelial lining of the urogenital sinus and ureteric bud responds to inductive signals from surrounding mesenchyme. Sonic hedgehog (Shh) signaling plays a pivotal role in this specification, expressed initially in the emerging urothelium and establishing an autoregulatory loop with transcription factors such as Foxa1 and Foxa2 to coordinate epithelial maturation and mesenchymal interactions.^[62] Basal cells, marking the progenitor layer, emerge first as a pseudostratified epithelium by week 8-10, followed by stratification into intermediate and superficial layers by week 12, when the transitional morphology becomes evident at a head-foot length of about 60 mm.^[63] Key transcription factors drive this stratification: Gata3 maintains endodermal identity and supports differentiation, Foxa1 regulates early patterning and decreases as superficial cells mature, and p63 (particularly the ΔNp63 isoform) is essential for basal cell proliferation and multilayered organization, with its absence leading to defective single-layered epithelium in model organisms.^[64] Hox genes, including Hoxa11, Hoxd11, and Hoxa13, contribute to regional patterning, ensuring proper transition from ureteric bud-derived urothelium to bladder lining by modulating branching morphogenesis and mesenchymal signaling.^[64] Developmental anomalies of the urothelium are uncommon but can arise from disruptions in cloacal partitioning or mesenchymal induction. Ectopic urothelium in the gastrointestinal tract, such as intestinal metaplasia extending into gut segments, occurs rarely in conditions like persistent cloaca, reflecting failed endodermal-mesodermal separation.^[65] The exstrophy-epispadias complex, with an incidence of approximately 1 in 30,000 live births for classic bladder exstrophy, results from ventral abdominal wall defects that evert the bladder, exposing and disrupting the immature urothelial lining to environmental factors and leading to metaplastic changes or ulceration.^[66] The embryological features of transitional epithelium were first described in human embryos by 19th-century anatomists, laying the groundwork for modern understanding. Recent studies (as of 2025) continue to build on these foundational insights, including refinements in the role of basal keratin 5-expressing cells as age-restricted progenitors and detailed mapping of epithelial differentiation in the urinary collecting system, which remain central to tissue engineering approaches for urothelial reconstruction.^[64]^[67]^[68] Stem cell roles contribute briefly to late maturation but are primarily postnatal.^[63]

Stem cell biology and tissue repair

The transitional epithelium, or urothelium, exhibits remarkable regenerative potential driven by a population of stem and progenitor cells primarily located in the basal layer. These basal cells, characterized by expression of keratins KRT5 and KRT14 (KRT5+/KRT14+), serve as key progenitors capable of self-renewal and differentiation into intermediate and superficial urothelial cells during homeostasis and injury response. Label-retaining cells (LRCs), which represent a subset of these basal progenitors with slow-cycling properties, contribute to long-term tissue maintenance, with urothelial turnover estimated at 3-6 months (approximately 90-180 days) in rodents and similar durations in humans under normal conditions.^[69] This quiescent state ensures barrier integrity but allows rapid activation upon perturbation. Wound healing in the urothelium involves coordinated basal cell proliferation, migration, and differentiation to restore multilayered architecture and functional specializations. Following injury, such as chemical or mechanical damage, KRT5+/TP63+ basal cells undergo hyperplasia and migrate to cover denuded areas, subsequently differentiating into intermediate cells that express markers like KRT7 and, ultimately, superficial umbrella cells bearing uroplakins for barrier reformation.^[70]^[71] Uroplakin expression, critical for the apical plaque barrier, is dynamically downregulated during acute injury but restored within 72 hours to 3 weeks post-injury, enabling full functional recovery in experimental models.^[72]^[73] Recent advances in regenerative medicine have leveraged induced pluripotent stem (iPS) cells to generate urothelial organoids, providing platforms for studying repair and potential transplantation. For instance, protocols from 2025 enable differentiation of human pluripotent stem cells into urothelial organoids via transient WNT signaling activation, recapitulating barrier formation and supporting disease modeling. Similarly, ureteral organoids derived from pluripotent stem cells have been developed to study upper tract development and regeneration. These iPS-derived organoids have been highlighted in tissue engineering reviews from 2023-2025 as promising tools for modeling regeneration and developing autologous therapies.^[74]^[75]^[76] Complementing this, biomaterials such as acellular matrices—decellularized scaffolds preserving extracellular matrix components—promote bladder repair by supporting host cell infiltration and urothelial regrowth, as demonstrated in a 2024 Frontiers in Bioengineering and Biotechnology study evaluating their functionalization for enhanced vascularization and reduced fibrosis.^[77] Despite these capabilities, challenges persist in urothelial repair, particularly due to the inherently slow basal turnover, which impairs sustained regeneration in chronic injuries like those from spinal cord injury or recurrent inflammation, often resulting in incomplete differentiation and persistent defects.^[78] Additionally, stem-like cells in the urothelium can contribute to tumor recurrence in pathological contexts by harnessing regenerative pathways for neoplastic expansion.00981-2) Experimental models have elucidated these dynamics, with rodent studies of chemical or surgical urothelial injury showing near-complete (over 90%) structural and functional recovery within 5-21 days through basal-driven mechanisms.^[79] In humans, emerging research includes stem cell-seeded scaffolds for urethral strictures, with preclinical studies and reviews from 2024-2025 highlighting their potential to prevent recurrence in tissue engineering applications.^[80] These models underscore the urothelium's parallels to embryonic progenitors in repair efficiency while highlighting translational potential.

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Apr 1, 2013 · Purinergic mechanisms ATP is released from both the apical and basolateral urothelial surfaces in response to bladder stretch and can act on ...
[40]
Receptors, channels, and signalling in the urothelial sensory system ...
Mar 1, 2016 · ATP seems to be the main messenger released from urothelial cells during purinergic mechanosensory transduction that acts on P2X3 receptors on ...
[41]
Urinary bladder urothelium: Molecular sensors of chemical/thermal ...
Recent findings support the view that the urothelium is a responsive structure capable of detecting mechanical, chemical and thermal stimuli in addition to ...
[42]
Expression and Antimicrobial Function of Beta-Defensin 1 in ... - NIH
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https://journals.physiology.org/doi/full/10.1152/ajpregu.00084.2024
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Interstitial Cystitis/Bladder Pain Syndrome - StatPearls - NCBI - NIH
IC/BPS patients with Hunner ulcers tend to be older with higher symptom scores, increased urinary frequency, more nocturia episodes, smaller voided volumes, and ...
[45]
Increased bladder permeability in interstitial cystitis/painful bladder ...
IC is the disorder most closely associated with loss of bladder permeability. Although IC can appear at any age, it becomes more common in women, during middle ...
[46]
Interstitial Cystitis: Practice Essentials, Background, Pathophysiology
Nov 18, 2024 · Current studies estimate that 2.7% to 6.5% of women in the United States have symptoms consistent with a diagnosis of interstitial cystitis/ ...
[47]
Hunner's lesions - PMC - NIH
Hunner's ulcers represent the minority of IC/PBS cases, typically less than 7% of patients. Moreover, this study mirrors others in that Hunner's ulcers ...Missing: BPS | Show results with:BPS
[48]
Keratinizing squamous metaplasia of the bladder: a review - PubMed
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[49]
Precursor Lesions of the Urinary Bladder - PubMed
This review discusses precursor lesions of urothelial, squamous and glandular lineage. For urothelial neoplasia, both flat lesions with atypia and early ' ...
[50]
Radiation cystitis - Bladder & urothelial tract - Pathology Outlines
Mar 26, 2024 · Radiation cystitis is inflammation of the urinary bladder caused by radiation therapy for pelvic malignancies.
[51]
Clinical Guidelines for the Prevention and Treatment of Radiation ...
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[52]
A bioengineered human urothelial organoid model reveals the urine ...
Oct 30, 2025 · By optical microscopy, we identified a population of bacteria that co-localise with the tissue after removing the urinary bacterial population ...
[53]
Altered urothelial ATP signaling in a major subset of human ...
Basal ATP release from the urothelium of OAB patients with pyuria was inhibited by the P2 receptor antagonist suramin and abolished by the hemichannel blocker ...
[54]
Mechanisms of hemorrhagic cystitis - PMC - NIH
Chemical cystitis can be caused by many classes of medications but is most commonly caused by intravenous chemotherapeutic treatment for breast cancer and ...Missing: transitional | Show results with:transitional
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Bladder Stones - StatPearls - NCBI Bookshelf
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Advancements in the management of overactive bladder in women ...
Jan 21, 2025 · Intravesical injections of botulinum toxin type A (BTX-A) are effective for treating refractory overactive bladder (OAB) in women.
[57]
Does cystoscopy method affect the investigation of bladder pain ...
The ESSIC recommends three bladder biopsies to be taken during cystoscopy and assessed for increased mast cell counts (MCCs) or MCs in the detrusor muscle [4].
[58]
Are Mast Cells Still Good Biomarkers for Bladder Pain Syndrome ...
ESSIC identifies mast cell infiltrates of detrusor muscle as a diagnostic criterion for bladder pain syndrome/interstitial cystitis.Missing: Hunner's ulcers
[59]
Embryology, Genitourinary - StatPearls - NCBI Bookshelf - NIH
The urogenital system is formed from intermediate mesoderm, while the lining of the urethra, urinary bladder, and reproductive system is composed of endoderm.Missing: membrane rupture
[60]
Differential transcription factor expression by human epithelial cells ...
... urothelium: a transitional epithelium. Urothelium derives from two embryological sources: bladder urothelium is endodermally-derived from the urinogenital ...Missing: cloaca Shh p63 Hox
[61]
Foxa1 and Foxa2 orchestrate development of the urethral tube and ...
Sep 1, 2020 · Foxa1 and Foxa2 orchestrate development of the urethral tube and division of the embryonic cloaca through an autoregulatory loop with Shh.Missing: transitional origin Gata3 p63 Hox
[62]
Urinary Bladder Development - Embryology
### Summary of Urothelium/Transitional Epithelium Development in the Urinary Bladder
[63]
Systematic Review to Compare Urothelium Differentiation with ...
Sonic hedgehog (Shh) is one of the factors important for the smooth muscle layer differentiation in mice22 and in humans. Shh is expressed in different types ...
[64]
The embryology of persistent cloaca and urogenital sinus ...
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[65]
The Exstrophy-epispadias complex - PMC - PubMed Central - NIH
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[66]
History - Embryologists - UNSW Embryology
Mar 26, 2020 · Much of the early history of embryology was European based and in the 19th Century mainly German researchers began the detailed description of human ...<|control11|><|separator|>
[67]
Proliferation and regeneration of the healthy human urothelium
Jun 20, 2025 · It is a slow regenerating tissue with a turnover time of 3 to 6 months [1–3]. However, after injury there is an enormous regeneration capability ...
[68]
KRT5high TP63-expressing urothelial basal cells act as a driver to ...
Jun 7, 2025 · We demonstrated that a sub-population of p63 positive basal cells could be activated and differentiate into intermediate and superficial umbrella cells.Missing: Shh | Show results with:Shh
[69]
Gliding Basal Cell Migration of the Urothelium during Wound Healing
In vivo time-lapse imaging revealed that, even in the absence of a wound, urothelial cells continuously moved and sometimes glided as a sheet over the ...
[70]
Uroplakins in the Lower Urinary Tract - PMC - NIH
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[71]
Expressions of Uroplakins in the Mouse Urinary Bladder with ...
Jul 30, 2009 · This study demonstrates a dynamic process, an extensive reduction and rapid recovery, for the UPs expression of the mouse urinary bladder after ...<|separator|>
[72]
Current Progress of Tissue Engineering With Stem Cells in Urology ...
Aug 7, 2025 · The risk of tumor formation remains a major concern in iPSC-derived constructs, especially in complex organoids subjected to multi-lineage ...
[73]
Recent advances in innovative biomaterials for promoting bladder ...
This article first summarized the latest research progress in the processing approaches and functionalization of acellular matrix, hydrogels, nanomaterials, and ...
[74]
Urothelial proliferation and regeneration after spinal cord injury - PMC
The presence of such cells even 28 days postinjury indicates that regeneration of the urothelium is altered by SCI.
[75]
Does the Urothelium of Old Mice Regenerate after Chitosan Injury ...
We discovered that the urothelial function restored comparably fast in both age groups and that the urothelium of young and old mice recovered within 5 days ...
[76]
Stem cell therapy for urethra and ureter tissue engineering
May 22, 2025 · The present study investigates the optimal stem cells for using in ureter and urethra tissue engineering by systematically reviewing the literature.Missing: patches phase