Activation of β-adrenoceptor signaling inhibits extracellular matrix deposition of human bladder smooth muscle cells
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA528287 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:To extensively explore its underlying mechanism, our study aims to investigate the effect of β-adrenoceptor (ADRB) signaling on the ECM of human bladder smooth muscle cells (hBSMCs) exposed to pathological hydrostatic pressure.
2022-03-20 | GSE128618 | GEO
Project description:We assessed the pivotal effect of YAP on the proliferation of human bladder smooth muscle cells (hBdSMCs) under different ECM stiffnesses. We investigated the interaction between YAP and Smad3 through mass spectrometry and immunoprecipitation (IP). Transcriptome sequencing was used to predict the phenotype and signalling pathways. CUT and TAG sequencing was utilized to analyse the target genes of Smad3, and a dual-luciferase reporter assay was used to confirm the sequencing results. The YAP inhibitor CA3 was used in a partial bladder outlet obstruction (pBOO) rat model construction to evaluate bladder smooth muscle proliferation in vivo.
2022-04-13 | PXD033188 |
Project description:Adult stem cells occupy a niche that contributes to their function but how stem cells remodel their microenvironment remains an open-ended question. Herein, biomaterials-based systems and metabolic labeling were utilized to evaluate how skeletal muscle stem cells and mesenchymal progenitors (fibro-adipogenic progenitors) deposit and remodel extracellular matrix. Differences in matrix production of muscle stem cells on substrates with different stiffness were then evaluated and linked with stem cell activation state. Reducing the ability to deposit new matrix attenuated function and mimicked impairments observed from muscle stem cells isolated in old age. Rescuing nascent protein deposition in old age stem cells with therapeutic supplementation rescued extracellular protein deposition and highlight how important this feature of niche remodeling is towards maintaining healthy stem cell function.
2024-02-15 | GSE252829 | GEO
Project description:Smooth muscle cells (SMCs) are important in a number of physiological systems and organs, including the cardiovascular system. The hallmark property of differentiated SMCs is the ability to contract, but contractile SMCs themselves show a range of phenotypes allowing prolonged tonic contraction in vascular smooth muscle or rapid phasic contraction in tissues such as bladder. Another distinctive characteristic, in contrast with terminally differentiated striated muscle cells, is that SMCs exhibit phenotypic plasticity. Vascular SMCs are able to modulate their phenotype along a continuum between a contractile phenotype, characteristic of healthy blood vessels, and a more proliferative âsyntheticâ phenotype, so-named for the enhanced synthesis and secretion of extracellular matrix components. Synthetic phenotype cells are found in a number of pathological situations such as atherosclerosis and arterial injury. We used mouse exon-junction (MJAY) arrays to gain insights into both the global contribution of alternative splicing events in re-shaping the transcriptome of dedifferentiating mouse aorta and bladder SMCs, and into the underlying regulatory mechanisms of the alternative splicing program. Affymetrix splice junction arrays (MJAY) were used to profile changes in both alternative splicing and transcript levels during the phenotypic modulation of smooth muscle cells when placed in culture. RNA extracted from intact aorta and bladder smooth muscle tissue was used for differentiated samples. For dedifferentiated, proliferative samples smooth muscle cells were enzymatically dispersed and grown in tissue culture for a week. Triplicate RNA samples were prepared from smooth muscle tissue of mouse aorta and bladder (differentiated) and from smooth muscle cells from each tissue cultured for 7 days (proliferative). The samples allowed comparison of alternative splicing (and other transcriptome) changes between differentiated and proliferative smooth muscle cell samples from two distinct types of smooth muscle cell, as well as allowing direct comparison of aorta (tonic smooth muscle) and bladder (phasic smooth muscle).
2016-07-01 | E-MTAB-4841 | biostudies-arrayexpress
Project description:Hypertrophic scars (HTS) are fibrotic skin disorders characterized by excessive deposition of dermal extracellular matrix (ECM), presenting significant challenges in clinical management despite incomplete understanding of their underlying mechanisms. Using MeRIP-seq and RNA-seq, our study initially revealed the direct regulatory role of ALKBH5 on ECM components in dermal fibroblasts, thereby involving in the pathogenesis of HTS.
2024-09-13 | GSE264515 | GEO
Project description:ALKBH5-mediated m6A demethylation ameliorates extracellular matrix deposition in cutaneous pathological fibrosis
| PRJNA1102882 | ENA
Project description:We show that Mustn1 (Musculoskeletal embryonic nuclear protein 1, also known as Mustang) is highly expressed in skeletal muscle during the early stages of hindlimb reloading. Mustn1 expression is transiently elevated in mouse and human skeletal muscle in response to intense exercise, resistance exercise, or injury. We find that Mustn1 expression is highest in smooth muscle-rich tissues, followed by skeletal muscle fibers. Muscle from heterozygous Mustn1-deficient mice exhibit differences in gene expression related to the extracellular matrix and cell adhesion, compared to wild-type littermates. Mustn1-deficient mice have normal muscle and aorta function and whole-body glucose metabolism. Loss of Mustn1 in vascular smooth muscle cells does not affect their proliferative or migratory functions. We show that Mustn1 can be secreted from smooth muscle cells, and that it is present in arterioles of the muscle microvasculature and in muscle interstitial fluid, in particular during the hindlimb reloading phase. Proteomics analysis of muscle from Mustn1-deficient mice confirms differences in extracellular matrix composition, and female mice display higher collagen content after chemically induced muscle injury compared to wild-type littermates.
2024-05-23 | PXD047169 | Pride
Project description:Hypertrophic scars (HTS) are fibrotic skin disorders characterized by excessive deposition of dermal extracellular matrix (ECM), presenting significant challenges in clinical management despite incomplete understanding of their underlying mechanisms. Using MeRIP-seq and RNA-seq, our study initially revealed the direct regulatory role of ALKBH5 on ECM components in dermal fibroblasts, thereby involving in the pathogenesis of HTS.
2024-09-13 | GSE264743 | GEO
Project description:SILAC analysis of human primary bladder smooth muscle cells treated with platelet-derived growth factor for 0, 4, and 24 h. Platelet-derived growth factor-BB (PDGF-BB) is a mitogen and motogen that has been implicated in the proliferation, migration and synthetic activities of smooth muscle cells (SMC) that characterize pathologic tissue remodeling in hollow organs. To explore the signals induced by PDGF on a global scale, we performed expression profiling and quantitative proteomics analysis of PDGF-treated human visceral SMC. 1695 genes and 241 proteins were identified as differentially expressed in PDGF-treated primary bladder SMC versus non-treated cells. Analysis of gene expression data revealed MYC, JUN, EGR1, MYB and RUNX1 as the transcription factors most significantly networked with upregulated genes; DDIT3, NFAT5, and SOX5 were most networked with downregulated genes. For protein identification and quantification, raw mass spectrometric data were analyzed with MaxQuant software (version 1.0.13.13). The parameters were set as follows. In the Quant module, SILAC triplets was selected; oxidation (M) and acetyl (Protein N-term) were set as variable modification; carbamidomethyl (C) was set as fixed modification; concatenated IPI human database (version 3.52) (74,190 forward sequences and 74,190 reverse sequences) was used for database searching; all other parameters were default. Tandem mass spectra were searched by Mascot (version 2.2.0.4) (Matrix Science, Boston, MA). In the Identify module, all parameters were default, except that maximal peptide posterior error probability was set as 0.05. False discovery rates for protein and peptide identifications were both set at 0.01.
2014-08-04 | PXD000624 | Pride
Project description:Quantification of local matrix deposition during muscle stem cell activation using engineered hydrogels
| PRJNA1062785 | ENA