Project description:To explore global molecular changes in smooth muscle in response to PDGFR activation, primary human bladder smooth muscle cells were treated with 1 nM PDGF-BB (hereafter PDGF) for 0, 4 or 24 h. Total RNA were prepared, and analyzed using expression profiling, and subjected to bioinformatic and functional interrogation. To identify molecular signatures of bladder smooth muscle peturbed by PDGF, primary human bladder smooth muscle cells were treated with 1 nM PDGF-BB (hereafter PDGF) for 0, 4 or 24 h.
Project description:In order to further study the role of circular RNA in the phenotypic transformation of vascular smooth muscle cells (VSMCs), the differential expression profile of circRNA in the phenotypic transition of VSMCs induced by platelet-derived growth factor-BB (PDGF-BB) was screened using chip technology. Vascular smooth muscle cells from rat thoracic aorta were induced with 20ng/ml PDGF-BB as the experimental group and compared with the control group. After induction for 24 hours, the differentially expressed circRNA was screened by circular RNA chip.
Project description:Smooth muscle cells were treated with platelet derived growth factor (PDGF-BB) and S100A4 protein to decipher the mechanisms by which they contribute to smooth muscle cell phenotypic transition. We report that PDGF-BB treatment upregulates genes related to growth response or to extracellular matrix component proteases, while S100A4 upregulates pro-inflammatory genes. When used in combination, PDGF-BB and S100A4 show synergistic action by enhancing the upregulation of genes already affected by S100A4 and by inducing the upregulation of genes exclusive for this condition.
Project description:To explore global molecular changes in smooth muscle in response to PDGFR activation, primary human bladder smooth muscle cells were treated with 1 nM PDGF-BB (hereafter PDGF) for 0, 4 or 24 h. Total RNA were prepared, and analyzed using expression profiling, and subjected to bioinformatic and functional interrogation.
Project description:To explore the potential involvement of tRNA derived fragments (tRFs) in the human aortic vascular smooth muscle cells (HASMCs), we conducted tRFs profiling in three pairs of differentiated HASMCs (treated with PBS) and dedifferentiated HASMCs (treated with PDGF-BB 50 ng/ml) by microarray. Our results showed that tRFs were aberrantly expressed in dedifferentiated HASMCs compared with differentiated HASMCs and provided potential targets for novel insights into VSMC differentiation or vascular remodeling diseases.
Project description:This experiment tests the hypothesis that interleukin-1 promotes SMC phenotypic modulation to a distinct inflammatory state relative to the growth factor PDGF-DD. Cultured rat aortic smooth muscle cells were treated with IL-1b (2.5 ng/mL) or vehicle (0.1% BSA and 10 mM acetic acid) or PDGF-DD (30 ng/mL) or vehicle (0.01% BSA) for 24 hours prior to harvest (n=1).
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.
Project description:We report the application of small RNA sequencing for high-throughput profiling of small RNA under 75 bp in vascular smooth muscle cell. By a reading depth of 30M and single stranded sequencing, we generated the small RNA signature on differentiated and de-differentiated vascular smooth muscle cell induced by PDGF-BB and H3K4me2 editing. We found that PDGF-BB and H3K4me2 editing induced de-differentiation modulated miRNA profile significantly, which was demonstrated at least in part responsible for modulated vascular smooth muscle cell phenotype.