ArticleNeurourology and urodynamics2020
LPS-mediated release of ATP from urothelial cells occurs by lysosomal exocytosis.
Article in Neurourology and urodynamics, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 19 citations in OpenAlex.
- Exocytosed ATP as a therapeutic target for inflammatory and metabolic diseases.Frontiers in pharmacology · 2026Review
- Mechanosensitive release of ATP in the urinary bladder mucosa.Purinergic signalling · 2025Review
- A microbiota-based perspective on urinary stone disease: insights from 16S rRNA sequencing and machine learning models.Frontiers in cellular and infection microbiology · 2025Article
- Article
- PDE5 inhibitor potentially improves polyuria and bladder storage and voiding dysfunctions in type 2 diabetic rats.PloS one · 2024Article
- Identification of circRNA-miRNA-mRNA network as biomarkers for interstitial cystitis/bladder pain syndrome.Aging · 2023Article
- Purinergic signaling: A new front-line determinant of resistance and susceptibility in leishmaniasis.Biomedical journal · 2022Review
- Review
- Paneth Cell Secretion in vivo Requires Expression of Tmem16a and Tmem16f.Gastro hep advances · 2022Article
- The nitric oxide-cyclic guanosine monophosphate pathway inhibits the bladder ATP release in response to a physiological or pathological stimulus.Physiological reports · 2021Article
- Lysosomes and Cancer Progression: A Malignant Liaison.Frontiers in cell and developmental biology · 2021Review
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
backgroundWhile numerous studies have confirmed ATP's importance in bladder physiology/pathophysiology, the literature is still conflicted regarding the mechanism of ATP release from the urothelium. Multiple mechanisms have been identified including non-vesicular release via pannexin channels as well as vesicular release via a mechanism blocked by botulinum toxin. Recently, it has been shown that lysosomes contain significant stores of ATP which can be released extracellularly in response to Toll-like receptor (TLR) stimulation.
objectiveThe goal of the current study was to determine if lysosomal exocytosis occurs in urothelial cells in response to TLR4 stimulation by its agonist, bacterial lipopolysaccharide (LPS). MATERIALS AND
methodsHuman urothelial cells from an immortalized cell line (TRT-HU1) were treated with bacterial LPS (100 μg/ml) or the nicotinic agoinist cytisine (100 μM) and extracellular release of ATP and lysosomal acid phosphatase were measured. Pannexin-mediated ATP release and lysosomal ATP release were differentiated using Brilliant Blue FCF to inhibit pannexin channels and glycyl-l-phenylalanine-β-naphthylamide (GPN) to destroy lysosomes. The mechanisms controlling lysosomal exocytosis were examined using lysosomal pH measurements using LysoSensor dye and intracellular calcium signaling using Fura-2.
resultsStimulation of TRT-HU1 cells with LPS significantly increased ATP release, which was inhibited by GPN, but not by Brilliant Blue FCF. Conversely, stimulation with cytisine induced ATP release that was sensitive to Brilliant Blue FCF but not GPN. LPS stimulation also induced the release of the lysosomal acid phosphatases. LPS increased lysosomal pH and direct alkalization of lysosomal pH using chloroquine or bafilomycin A1 induced ATP and acid phosphatase release, indicating an important role for pH in lysosomal exocytosis. Additionally, stimulation of lysosomal transient receptor potential mucolipin 1 calcium channels evoked intracellular calcium transients as well as ATP release.
conclusionThese data indicate that LPS-induced ATP release from urothelial cells is mediated by lysosomal exocytosis, a vesicular mechanism distinctly separate from non-vesicular release via pannexin channels.
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