Ontology highlight
ABSTRACT:
PROVIDER: PRJNA856421 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR20012900_1.fastq.gz | Fastqsanger.gz | |||
| SRR20012900_2.fastq.gz | Fastqsanger.gz | |||
| SRR20012901_1.fastq.gz | Fastqsanger.gz | |||
| SRR20012901_2.fastq.gz | Fastqsanger.gz | |||
| SRR20012902_1.fastq.gz | Fastqsanger.gz |
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Project description:Extracellular stiffness and urinary bladder fibrosis
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Project description:<p>Mechanical force is critical for the development and remodeling of bone. Here we report that mechanical force regulates the production of the metabolite asymmetric dimethylarginine (ADMA) via regulating the hydrolytic enzyme dimethylarginine dimethylaminohydrolase 1 (Ddah1) expression in osteoblasts. The presence of -394 4N del/ins polymorphism of Ddah1 and higher serum ADMA concentration are negatively associated with bone mineral density. Global or osteoblast-specific deletion of Ddah1 leads to increased ADMA level but reduced bone formation. Further molecular study unveils that mechanical stimulation enhances TAZ/SMAD4-induced Ddah1 transcription. Deletion of Ddah1 in osteoblast-lineage cells fails to respond to mechanical stimulus-associated bone formation. Taken together, the study reveals mechanical force is capable of down-regulating ADMA to enhance bone formation.</p>
2021-11-23 | MTBLS3725 | MetaboLights
Project description:Urinary bladder wound healing is today pooorly chracterized. MicroRNAs are small non-coding RNA molecules with regulatory functions. In this study we aimed at identifying microRNAs expressed during bladder wound healing. We performed Affymetrix microRNA profiling of the rodent urinary bladder during healing of a surgically created wound.
2021-12-01 | GSE176515 | GEO
Project description:We compared the chnages in urinary bladder and iliac lymph nodes microRNAs in the control and experimental autoimmune cystitis in mice. A set of urinary bladder microRNAs (miRNAs) shows profound upregulation or downregulation in the expression profiles of the experimental IC as compared to control.
2021-06-12 | GSE177066 | GEO
Project description:Hypertrophic scar (HTS) formation is characterized by exuberant fibroproliferation for reasons that remain poorly understood1. One important but often overlooked component of wound repair is mechanical force, which regulates reciprocal cell-matrix interactions through focal adhesion components including focal adhesion kinase (FAK)1,2. Here we report that FAK is activated following cutaneous injury and that this activation is potentiated by mechanical loading. Transgenic mice lacking fibroblast-specific FAK exhibit significantly less fibrosis in a preclinical model of HTS formation. Inflammatory pathways involving monocyte chemoattractant protein-1 (MCP-1), a chemokine highly implicated in human skin fibrosis3, are triggered following FAK activation, mechanistically linking physical force to fibrosis. Further, small molecule inhibition of FAK effectively abrogates fibroproliferative mechanisms in human cells and significantly reduces scar formation in vivo. Collectively, these findings establish a molecular basis for HTS formation based on the mechanical activation of fibroblast-specific FAK and demonstrate the therapeutic potential of targeted mechanomodulatory strategies. Wildtype murine tissue was harvested at either day 6 or 14 post-injury following 48 hours or 10 days of mechanical loading, respectively (n=4 mice per group per time point). Murine RNA was isolated, labeled, and hybridized to the GeneChip microarray according to the manufacturer’s protocols (Affymetrix, Santa Clara, CA, USA). Each gene in the microarray was represented by 20 oligonucleotide pairs, with each pair consisting of an oligonucleotide perfectly matched to the cDNA sequence, and a second oligonucleotide containing a single base mismatch. Raw microarray data (sample intensity files) were processed using GeneSpring GX 11.0 (Agilent Technologies Inc., Santa Clara, CA, USA).
2011-01-14 | E-GEOD-26390 | biostudies-arrayexpress
Project description:The gene expression profling between non-treated urinary bladder epithelium (Control) and dimethylarsinic acid-induced urinary bladder tumors of F344 male rats.
2023-08-09 | GSE207973 | GEO
Project description:Lower urinary tract symptoms (LUTS) refer to a spectrum of urological diseases, and incomplete bladder emptying is common among affected patients. The etiology of LUTS is largely unknown and evidence arising from epidemiologic, clinical, and basic research suggests that bladder fibrosis is an important contributing factor to pathogenesis of LUTS. MicroRNAs (miRNAs) are short (~22 nucleotides), non-coding RNAs that repress target gene expression by a combination of mRNA degradation and translation inhibition. The miR-29 family is best known for its anti-fibrotic role in various organs. Recent studies have reported decreased miR-29 in bladders of patients with outlet obstruction and in a rat model of bladder outlet obstruction, suggesting that miR-29 may be associated with impaired bladder function subsequent to tissue fibrosis. In the present study, we characterized bladder function in male mice lacking expression of MIR29A and MIR29B1 (miR-29a/b1). We found that lack of miR-29a/b1 resulted in severe urinary retention, increased urination duration with reduced flow rate, and these mice failed to void or voided irregularly during anesthetized cytometry. Collagens and elastin were increased in the bladder walls of mice lacking miR-29a/b1. These findings reveal an important role of mir-29 in bladder homeostasis and suggest therapeutic potential of miR-29 to improve symptoms in patients with LUTS.
2023-05-16 | GSE218946 | GEO
Project description:Analysis of urinary bladder in wild-type C57BL/6 females sacrificed every 4 hours at six time points under constant darkness after acclimation for 2 weeks under 12-hour light and 12-hour dark conditions. Results provide insight into circadian gene expression patterns in normal urinary bladder. Analysis of urinary bladder in wild-type C57BL/6 females sacrificed every 4 hours at six time points (n=2 for each time (CT 0, 4, 8, 12 and 20)) under constant darkness after acclimation for 2 weeks under 12-hour light and 12-hour dark conditions.
2012-04-30 | E-GEOD-35795 | biostudies-arrayexpress
Project description:Hypertrophic scar (HTS) formation is characterized by exuberant fibroproliferation for reasons that remain poorly understood1. One important but often overlooked component of wound repair is mechanical force, which regulates reciprocal cell-matrix interactions through focal adhesion components including focal adhesion kinase (FAK)1,2. Here we report that FAK is activated following cutaneous injury and that this activation is potentiated by mechanical loading. Transgenic mice lacking fibroblast-specific FAK exhibit significantly less fibrosis in a preclinical model of HTS formation. Inflammatory pathways involving monocyte chemoattractant protein-1 (MCP-1), a chemokine highly implicated in human skin fibrosis3, are triggered following FAK activation, mechanistically linking physical force to fibrosis. Further, small molecule inhibition of FAK effectively abrogates fibroproliferative mechanisms in human cells and significantly reduces scar formation in vivo. Collectively, these findings establish a molecular basis for HTS formation based on the mechanical activation of fibroblast-specific FAK and demonstrate the therapeutic potential of targeted mechanomodulatory strategies.
2011-01-14 | GSE26390 | GEO
Project description:The aim of this cDNA array study is to search for advanced markers related to the pathogenesis of ketamine-induced cystitis. The result revealed a number of gene expressions involved in chronic wound healing response and collagen accumulation, which were closely related to fibrosis progression in the connective tissue of mice urinary bladder.
2016-05-01 | GSE68539 | GEO