Activation of β-adrenoceptor signaling inhibits extracellular matrix deposition of human bladder smooth muscle cells
Ontology highlight
ABSTRACT:
ORGANISM(S): Rattus norvegicus
PROVIDER: GSE128618 | GEO | 2022/03/20
REPOSITORIES: GEO
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Project description:Activation of β-adrenoceptor signaling inhibits extracellular matrix deposition of human bladder smooth muscle cells
| PRJNA528287 | ENA
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:Urothelial carcinoma (UC) is the most common histologic subtype of bladder cancer. The administration of mitomycin C (MMC) into bladder after transurethral resection of the bladder tumor (TURBT) is a common treatment strategy for preventing recurrence after surgery. We previously applied hydrostatic pressure combined with MMC in UC cells and found that hydrostatic pressure synergistically enhanced MMC-induced UC cell apoptosis via the Fas/FasL pathways. To understand the alteration of gene expressions in UC cells caused by hydrostatic pressure and MMC, oligonucleotide microarray was used to explore all of the differentially expressed genes. After bioinformatics analysis and gene annotation, Toll-like receptor 6 (TLR6) and connective tissue growth factor (CTGF) showed significant up-regulation among altered genes, and their expressions with each treatment of UC cells were validated by quantitative real-time PCR (qPCR). We conclude that under treatment with MMC and hydrostatic pressure, UC cells showed increasing apoptosis via extrinsic pathways through upregulation of TLR6 and CTGF.
2016-03-21 | GSE45385 | GEO
Project description:Hydrostatic pressure is one of the physical factors affecting cellular physiology. Hydrostatic pressure of a few hundred MPa decreases the viability of yeast cells, and pressure of a few tens MPa decreases the growth rate. To understand the effect of hydrostatic pressure, we employed yeast, Saccharomyces cerevisiae, DNA microarrays and analyzed genome-wide mRNA expression profiles under hydrostatic pressures. In this experiment, we selected a hydrostatic pressure of 30 MPa at 25 degrees C because yeast cells are able to grow with this condition. Keywords: stress response
2007-11-01 | GSE9403 | GEO
Project description:Hydrostatic pressure is one of the physical factors affecting cellular physiology. Hydrostatic pressure of a few hundred MPa decreases the viability of yeast cells, and pressure of a few tens MPa decreases the growth rate. To understand the effect of hydrostatic pressure, we employed yeast, Saccharomyces cerevisiae, DNA microarrays and analyzed genome-wide mRNA expression profiles under hydrostatic pressures. In this experiment, we selected a hydrostatic pressure of 40 MPa at 25 degrees C because the condition is not lethal for yeast cells but the growth was suppressed. Keywords: stress response
2007-11-01 | GSE9406 | GEO
Project description:Hydrostatic pressure is one of the main mechanical stimuli cartilage cells are submitted to during joint loading. If moderate hydrostatic pressure is known to be beneficial to cartilage differentiation, excessive pressure, on the other hand, induces changes in cartilage similar to those observed in osteoarthritic cartilage. Therefore, the purpose of the experiment is to identify new target genes of high hydrostatic pressure in chondrocyte precursor cells.
2017-12-02 | E-MTAB-5326 | biostudies-arrayexpress
Project description:A major problem in cancer research is the lack of a tractable model for delayed metastasis. Herein we show that cancer cells suppressed by SISgel, a gel-forming normal ECM material derived from Small Intestine Submucosa, in flank xenografts show properties of suppression and re-activation that are very similar to normal delayed metastasis and suggest they can serve as a novel model for developing therapeutics to target micrometastases or suppressed cancer cells. Co-injection with SISgel suppressed the malignant phenotype of highly invasive J82 and T24 bladder cancer cells and highly metastatic JB-V cells in flank xenografts. Cells could remain viable up to 120 days without forming tumors and appeared much more highly differentiated and less atypical than tumors from cells co-injected with Matrigel. In 40% of SISgel xenografts, growth resumed in the malignant phenotype after a period of suppression or dormancy for at least 30 days and was more likely with implantation of 3 million cells or more cells. Ordinary Type I collagen did not suppress malignant growth, and tumors developed about as well with collagen as with Matrigel. A clear signal in gene expression over different cell lines was not seen, but in contrast, Reverse Phase Protein Analysis of 250 proteins across 4 cell lines identified a clear signal at the protein level involving Integrin Linked Kinase (ILK) signaling that was confirmed by an ILK inhibitor. We suggest that cancer cells suppressed on SISgel could serve as a model for dormancy and re-awakening to develop therapeutic targets for micrometastases. Earlier we demonstrated that the phenotype of bladder cancer cells was radically different in 3-dimensional organotypic culture when grown on a normal extracellular matrix preparation (SISgel) as compared to that observed on a cancer-modulated permissive extracellular matrix preparation (Matrigel). SISgel is a gel-forming material derived from acellular small intestine submucosa, whereas Matrigel is a basement membrane preparation obtained from a mouse sarcoma. On Matrigel the bladder cancer cells recapitulated the phenotype reported for the original tumor; in sharp contrast, most of the malignant properties were lost when the cells were grown on SISgel. Cell lines derived from papillomas formed a layered structure reminiscent of normal urothelium, whereas cell lines derived from higher grade tumors formed a noninvasive layer of cells. These findings suggested that growth of cancer cells on normal ECM could provide a model to investigate the phenomenon of suppression of malignancy by normal ECM in metastasis and recurrence. In this study we explored whether the phenotypic suppression seen in organotypic culture of bladder cancer cells on SISgel also is observed in vivo. Positive findings support the use of SISgel as a model for investigations of the dormant or suppressed tumor cell phenotype and of mechanisms by which the normal ECM exerts an inhibitory influence on tumorigenesis and metastasis. The findings strongly suggest that interactions of cancer cells with normal ECM play an important role in recurrence and metastasis and further suggest that targeting suppressed cells could represent a heretofore unexploited point of vulnerability in cancer therapy.
2014-02-20 | E-GEOD-35947 | biostudies-arrayexpress
Project description:This SuperSeries is composed of the following subset Series: GSE28410: Mouse oocytes: High hydrostatic pressure (HP) treated vs. Control GSE28411: Mouse in vitro fertilized four-cell stage embryos: High hydrostatic pressure (HP) treated vs. Control Refer to individual Series
2012-01-06 | E-GEOD-28443 | biostudies-arrayexpress
Project description:This study was undertaken to identify how gene expression of the RT4 bladder papilloma cells respond to extracellular matrics (ECM) Matrigel. Gene expression profile of RT4 cells grown on Plastic was compared with expression profiles of RT4 cells grown on Matriges over 12 hours-9 days timecourse. Total 5881 hypervariable (HV) genes were found to vary significantly over the time points, indicating a response to matrix change. Correlational clustering showed these HV genes fell into distinct families, predominantly genes which became highly expressed on ECM. Another cluster show genes expressed at 12 hours after grown on Matrigel and third cluster show genes whose expression decreased below noise level on Matrigel. This indicate that processes responsible for cell adaptation to ECM happen within first 12 hours and the second cluster form last response of those active processes. Over 1-9 days of cell grows on Matrigel those genes are constantly expressed. Cell signaling and cellular growth and proliferation accounted for major functions for those genes. G-protein signaling, immune response and NF-kB signaling accounted for most dramatically affected canonical pathways. Genes sharing similar ontologies also share several overrepresented transcription regulatory elements confirmed by independent experiment on Panomics platform.Thus, rapid response for ECM orchestrated by several transcription factors was observed. Identified canonical pathways indicate possible targets for manipulating cell phenotype on ECM. Keywords: extracellular matrix, gene expression, RT4, Matrigel, microarray, time course
2008-06-10 | GSE9291 | GEO
Project description:Pulmonary artery (PA) pressure increases during lung growth after unilateral pneumonectomy (PNX). Mechanosensitive transcriptional co-activator, yes-associated protein (YAP1), in endothelial cells (ECs) is necessary for angiogenesis during post-PNX lung growth. We investigate whether increases in PA pressure following PNX controls angiogenesis through YAP1. When hydrostatic pressure is applied to human pulmonary arterial ECs (HPAECs), the expression of YAP1, transcription factor TEAD1, and angiogenic factor receptor Tie2 increases, while these effects are inhibited when HPAECs are treated with YAP1 siRNA or YAP1S94A mutant that fails to bind to TEAD1. Hydrostatic pressure also stimulates DNA synthesis and cell migration in HPAECs, while YAP1 knockdown or YAP1S94A mutant inhibits the effects. Gene enrichment analysis reveals that the levels of extracellular matrix (ECM) or cell adhesion molecules are altered in post-PNX mouse lung ECs, which interact with YAP1. Exosomes are known to promote tissue regeneration. Proteomics analysis reveals that exosomes isolated from conditioned media of post-PNX mouse lung ECs contain the higher levels of ECM and cell-adhesion proteins compared to those from sham-operated mouse lung ECs. Recruitment of host lung ECs and blood vessel formation are stimulated in the fibrin gel containing exosomes isolated from post-PNX mouse lung ECs or pressurized ECs, while YAP1 knockdown inhibits the effects. These results suggest that increases in PA pressure stimulate angiogenesis through YAP1 during regenerative lung growth.
2022-03-09 | GSE154110 | GEO