Fibroblast growth factor 2 promotes bladder hypertrophy caused by partial bladder outlet obstruction
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ABSTRACT:
PROVIDER: PRJNA704641 | ENA |
REPOSITORIES: ENA
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Project description:The current study aims to investigate molecular alterations and biomarkers associated with partial BOO (PBOO) in rats. RNA-seq analyses were conducted to identify molecular alterations. Rats with PBOO experienced hypertrophy of smooth muscle cells and hyperplasia of interstitial cells during the first 4 weeks after the initiation of obstruction. Four weeks later, rats with PBOO showed activation of the adaptive immune response, cell death and apoptosis. The levels of BDNF and FGF2 in the serum gradually increased in the first four weeks and gradually decreased after week 4. FGF2 levels slightly correlated with prostate volume (R=0.156, P=0.0028) but not with age or BMI in BPH patients. FGF2 is involved in the development of hypertrophy in the PBOO bladder and shows a positive correlation with prostate volume in BPH patients.
2021-04-20 | GSE167430 | GEO
Project description:Obstruction in any part between the outlet of the bladder and the external urethra is called partial Bladder outlet obstruction (pBOO), which is a common disease in urology, which may cause bladder dysfunction. We have comfirmed that human urine-derived stem cells (hUSCs) could improve the bladder function of pBOO rats in our previous study. We thus explored the role of miRNAs in pBOO rats before and after treatment of hUSCs, and revealed that they could serve as effective prevention and treatment therapeutic targets. Rat bladder tissues were used for miRNA sequencing. We identified 8 differentially expressed miRNAs in the pBOO rats before and after treatment of hUSCs.
2021-04-02 | GSE171293 | GEO
Project description:Obstruction in any part between the outlet of the bladder and the external urethra is called partial Bladder outlet obstruction (pBOO), which is a common disease in urology, which may cause bladder dysfunction. We have comfirmed that human urine-derived stem cells (hUSCs) could improve the bladder function of pBOO rats in our previous study. We thus explored the role of miRNAs in pBOO rats before and after treatment of hUSCs, and revealed that they could serve as effective prevention and treatment therapeutic targets. Rat bladder tissues were used for circRNA, lncRNA and mRNA sequencing.
2021-04-02 | GSE171366 | GEO
Project description:Recently, we described a nerve-sparing mid-urethra model of partial outlet obstruction (NeMO) that has high consistency and minimal mortalities, unlike the traditional model of obstruction proximal to the bladder neck. To uncover pathogenic pathways in PBO, we performed NeMO and examined the transcriptional responses in the bladder. NeMO increased bladder mass, relative bladder mass, hyperactivity and decreased voiding efficiency. In NeMO vs. sham bladders, there were 831 differentially expressed genes, which correlated significantly with physiologic parameters. Of the 796 genes mapped to human orthologues, upregulated genes were enriched for functions related to extracellular matrix, and cytokine activation, and downregulated genes were enriched for functions relating to muscle contraction and metabolism. To identify candidate drug targets for the treatment of PBO, we analysed the conserved transcriptional response to PBO in human and mouse. Gene sets related to cytokine activation, including the TNF pathway, were consistently upregulated in both human and mouse bladders affected by obstruction, revealing a potential therapeutic target. Accordingly, we depleted macrophages, which are an important source of TNF, with clodronate (CL). In NeMO, CL significantly decreased hyperactive voiding, residual volumes and improved voiding efficiency (p<0.05). Moreover, the expression levels of cytokines/chemokines correlated with several bladder functional parameters. Thus, genes that control progression of pathology in bladder obstruction are consistently dysregulated in NeMO and human bladders affected by PBO, supporting the use of the nerve-sparing mouse obstruction model for therapeutic exploration.
2022-07-27 | GSE209625 | GEO
Project description:Prostatic inflammation plays a role in the progression of benign prostatic hyperplasia (BPH). Eviprostat is an antiinflammatory and antioxidant phytotherapeutic agent widely used to treat lower urinary tract symptoms in BPH. However, because Eviprostat is a mixture of compounds from multiple natural sources, its mechanism of action has been difficult to investigate. In this study, we used oligonucleotide microarrays to identify changes in gene expression that occur in the prostate of rats with surgically induced partial bladder outlet obstruction and the effect of Eviprostat on those changes. Male rats were divided into four groups of five or six animals each. The rats in groups 1 and 2 underwent a sham operation. Five days after the sham operation, group 1 was treated twice a day with vehicle (0.1% (w/v) Tween 80; sham/vehicle group) and group 2 was treated twice a day with 18 mg/kg Eviprostat (36 mg/kg daily; sham/Eviprostat group). The rats in groups 3 and 4 underwent surgical partial bladder outlet obstruction. Briefly, with the rat in the supine position, a midline suprapubic incision was made and the bilateral prostate was retracted to expose the neck of the bladder and the urethra, care being taken not to damage the bladder. The loose connective tissue at the base of the bladder was dissected away from the proximal urethra. A rubber ring was cut open and placed around the proximal urethra, and a 4-0 silk ligature was tied around the rubber ring. From the day after the operation, group 3 was treated twice a day for five days with vehicle (operated/vehicle group) and group 4 was treated twice a day for five days with 18 mg/kg Eviprostat (36 mg/kg daily; operated/Eviprostat group). On the sixth day, 2 h after the last administration, the rats were sacrificed and the prostate was rapidly removed.
2010-04-09 | E-GEOD-16063 | biostudies-arrayexpress
Project description:The current study aims to investigate molecular alterations and biomarkers associated with partial BOO (PBOO) in rats.TMT-Labeling Proteomic Analysis of PBOO Bladder Tissues at Week 5.
2021-09-10 | PXD024378 | Pride
Project description:Prostatic inflammation plays a role in the progression of benign prostatic hyperplasia (BPH). Eviprostat is an antiinflammatory and antioxidant phytotherapeutic agent widely used to treat lower urinary tract symptoms in BPH. However, because Eviprostat is a mixture of compounds from multiple natural sources, its mechanism of action has been difficult to investigate. In this study, we used oligonucleotide microarrays to identify changes in gene expression that occur in the prostate of rats with surgically induced partial bladder outlet obstruction and the effect of Eviprostat on those changes.
2009-07-21 | GSE16063 | GEO
Project description: Not available
| S-EPMC8042216 | biostudies-literature
Project description:Urethra was partially ligated and the urinary bladder was removed 10 days or 6 weeks after obstruction. Sham operated rats were used as controls. An addtitonal group of rats were repoerated 6 weeks after surgery and the obstruction was removed. These rats were then sacrificed 10 days after deobstruction. The bladder (including the urothelium) was frozen and used for RNA extraction. Urinary bladders from sham-operated, 10 days and 6 weeks after obstruction and rats 10 days after deobstruction were compared. mRNA and microRNA were both analyzed.
2013-11-24 | E-GEOD-47080 | biostudies-arrayexpress
Project description:Leucine-rich-repeats and immunoglobulin-like-domains (LRIG2) variants can occur in urofacial syndrome (UFS), an inherited disease characterised by functional bladder outlet obstruction. We aimed to define the pathobiology underlying UFS which we hypothesised would illuminate how the bladder becomes innervated. Lrig2 was detected in pelvic ganglia supplying autonomic neurons to the bladder, and in neurites and glia emanating from explanted ganglia. One week old Lrig2 mutant mice displayed abnormally patterned bladder nerves, as did mice with mutations of Hpse2, also mutated in some UFS patients. From two weeks postnatally, Lrig2 mutants had urination defects resembling UFS. Molecules implicated in neural biology, including Nos1 which relaxes the bladder outlet, were dysregulated in newborn Lrig2 mutant bladders. These molecular aberrations preceded manifest urination defects. We discovered novel homozygous missense LRIG2 variants in non-syndromic bladder outlet obstruction. Molecules mutated in UFS are required for bladder innervation and LRIG2 variants can occur in non-syndromic bladder disease as well as in UFS.
2020-04-27 | E-MTAB-6089 | biostudies-arrayexpress