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Fibroblast growth factor 2 promotes bladder hypertrophy caused by partial bladder outlet obstruction

ABSTRACT: Fibroblast growth factor 2 promotes bladder hypertrophy caused by partial bladder outlet obstruction

PROVIDER: PRJNA704641 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13777510_1.fastq.gz	Fastqsanger.gz
	SRR13777510_2.fastq.gz	Fastqsanger.gz
	SRR13777511_1.fastq.gz	Fastqsanger.gz
	SRR13777511_2.fastq.gz	Fastqsanger.gz
	SRR13777512_1.fastq.gz	Fastqsanger.gz

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Fibroblast growth factor 2 promotes bladder hypertrophy caused by partial bladder outlet obstruction

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

The expression profile of miRNA in the bladder tissue of partial bladder outlet obstruction rats before and after treatment of human urine-derived stem cells

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

The expression profile of circRNA, lncRNA and mRNA in the bladder tissue of partial bladder outlet obstruction rats before and after treatment of human urine-derived stem cells

2021-04-02 | GSE171366 | GEO

De-obstruction of bladder outlet in humans reverses organ remodeling

Project description:Bladder outlet obstruction (BOO) causes lower urinary tract symptoms and objectifiable urodynamic changes in bladder function. We carried out an integrated transcriptome and proteome analysis of bladder samples from male patients with BOO before and 3 months after de-obstruction surgery (transurethral resection of the prostate, TURP). mRNA and protein profiles were correlated with urodynamic findings, specifically voiding detrusor pressure (PdetQmax) before TURP. Patients with high PdetQmax showed less advanced remodeling and inflammatory changes than those with lower values. We oberved significant dysregulation of gene expression, which was reversed by de-obstruction in both patients’ groups. We propose a series of biomarker genes, indicative of BOO, and possibly contributing to the bladder changes. Our data sheds light on the stages of progressive obstruction-induced bladder decompensation, and might add selecting the operation point to avoid the loss of contractility.

2024-05-21 | PXD044777 | Pride

Human - murine concordance of molecular signatures in nerve-sparing murine partial bladder outlet obstruction (NeMO)

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

Prostates of rats with induced partial bladder outlet obstruction and the effect of Eviprostat on those changes

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

Fibroblast growth factor 2 promotes bladder hypertrophy caused by partial bladder outlet obstruction

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

Prostates of rats with induced partial bladder outlet obstruction and the effect of Eviprostat on those changes

2009-07-21 | GSE16063 | GEO

Fibroblast Growth Factor 2 Promotes Bladder Hypertrophy Caused by Partial Bladder Outlet Obstruction.

Project description:Non-invasive biomarkers to identify patients with bladder outlet obstruction (BOO)-related dysfunction are still needed to guide clinical practice. The current study aims to investigate molecular alterations and biomarkers associated with partial BOO (PBOO) in rats. Sprague-Dawley rats were used to establish the BOO model. Serum samples from 60 patients with benign prostatic hyperplasia (BPH) were used for enzyme-linked immunosorbent assay analysis. RNA sequencing and TMT-labeling proteomic analyses were conducted to identify molecular alterations. Masson's trichrome, H&E, and immunohistochemical staining and western blotting were conducted by using conventional methods following the manufacturer's instructions. 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 brain-derived neurotrophic factor (BDNF) and fibroblast growth factor 2 (FGF2) in the serum gradually increased in the first 4 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. No correlations were found between BDNF levels and prostate volume, age or BMI. BOO induces a change from bladder compensation to decompensation at week 4. FGF2 is involved in the development of hypertrophy in the PBOO bladder and shows a positive correlation with prostate volume in BPH patients.

| S-EPMC8042216 | biostudies-literature

Molecular characterization of obstructive and neurogenic lower urinary tract dysfunction (LUTD) in SCI-induced and partial bladder outlet obstruction mouse models

Project description:SCI-induced and partial bladder outlet obstruction mouse models

| PRJEB58912 | ENA