ArticleAmerican journal of physiology. Renal physiology2012
Connective tissue and its growth factor CTGF distinguish the morphometric and molecular remodeling of the bladder in a model of neurogenic bladder.
Article in American journal of physiology. Renal physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
25 citing papers in PubMed, 1 synthesis or guideline pooled it, 44 citations in OpenAlex.
- Molecular Mechanism Operating in Animal Models of Neurogenic Detrusor Overactivity: A Systematic Review Focusing on Bladder Dysfunction of Neurogenic Origin.International journal of molecular sciences · 2023Pooled it
- Development of a machine learning model for predicting renal damage in children with closed spinal dysraphism.BMC pediatrics · 2025Article
- The association between magnesium depletion score (MDS) and overactive bladder (OAB) among the U.S. population.Journal of health, population, and nutrition · 2025Article
- Activation of the TGF-β1/Smads/α-SMA pathway is related to histological and functional changes in children with neurogenic bladder.Scientific reports · 2022Article
- Animal modeling of lower urinary tract dysfunction associated with multiple sclerosis: Part I: Justification of the mouse model for MS research.Neurourology and urodynamics · 2021Review
- PART 2: Mouse models for multiple sclerosis research.Neurourology and urodynamics · 2021Review
- MicroRNA-219c-5p regulates bladder fibrosis by targeting FN1.BMC urology · 2020Article
- Stretch- and carbachol-induced ATP release from bladder wall preparations of young and aged mice.Neurourology and urodynamics · 2020Article
- Detrusor contractility to parasympathetic mediators is differentially altered in the compensated and decompensated states of diabetic bladder dysfunction.American journal of physiology. Renal physiology · 2019Article
- Differential neurodegenerative phenotypes are associated with heterogeneous voiding dysfunction in a coronavirus-induced model of multiple sclerosis.Scientific reports · 2019Article
- Urinary bladder organ hypertrophy is partially regulated by Akt1-mediated protein synthesis pathway.Life sciences · 2018Article
- Concordant miRNA and mRNA expression profiles in humans and mice with bladder outlet obstruction.American journal of clinical and experimental urology · 2018Article
- Bladder fibrosis during outlet obstruction is triggered through the NLRP3 inflammasome and the production of IL-1β.American journal of physiology. Renal physiology · 2017Article
- Involvement of interstitial cells of Cajal in bladder dysfunction in mice with experimental autoimmune encephalomyelitis.International urology and nephrology · 2017Article
- Bladder wall thickness in the assessment of neurogenic bladder: a translational discussion of current clinical applications.Annals of translational medicine · 2016Article
- Inhibition of NMDAR reduces bladder hypertrophy and improves bladder function in cyclophosphamide induced cystitis.The Journal of urology · 2015Article
- Research Findings on Overactive Bladder.Current urology · 2015Review
- The potential role of stem cells in the treatment of urinary incontinence.Therapeutic advances in urology · 2015Review
- The urinary bladder of spontaneously hypertensive rat demonstrates bladder hypertrophy, inflammation, and fibrosis but not hyperplasia.Life sciences · 2015Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
We previously reported that mice with experimental autoimmune encephalomyelitis (EAE), a model of multiple sclerosis (MS), develop profound urinary bladder dysfunction. Because neurogenic bladder in MS patients causes marked bladder remodeling, we next examined morphometric and molecular alterations of the bladder in EAE mice. EAE was created in female SJL/J mice by immunization with the p139-151 encephalitogenic peptide of myelin proteolipid protein in complete Freund's adjuvant, along with intraperitoneal injections of Bordetella pertussis toxin. Seventy days after immunization, mice were scored for the level of neurological impairment and then killed. Spinal cord sections were assessed for demyelination, inflammation, and T cell infiltration; the composition of the bladder tissue was measured quantitatively; and gene expression of markers of tissue remodeling and fibrosis was assessed. A significant increase in the bladder weight-to-body weight ratio was observed with increasing neurological impairment, and morphometric analysis showed marked bladder remodeling with increased luminal area and tissue hypertrophy. Despite increased amounts of all tissue components (urothelium, smooth muscle, and connective tissue), the ratio of connective tissue to muscle increased significantly in EAE mice compared with control mice. Marked increases in mRNA expression of collagen type I α(2), tropoelastin, transforming growth factor-β3, and connective tissue growth factor (CTGF) were observed in EAE mice, as were decreased levels of mRNAs for smooth muscle myosin heavy chain, nerve growth factors, and muscarinic and purinergic receptors. Our results suggest that bladder remodeling corresponding to EAE severity may be due to enhanced expression of CTGF and increased growth of connective tissue.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.