Project description:Streptococcus pneumoniae (Spn) is a major causative organism of empyema, an inflammatory condition occurring in the pleural sac. In this study, we used Spn cDNA microarrays to characterize the transcriptional responses occurring during initial contact between Spn and a human pleural mesothelial cell line (PMC) in vitro
Project description:Mesothelial cells, which interact with endothelial cells, are widely used in research including cancer and drug development, have not been comprehensively profiled. We therefore performed RNA sequencing of polarized, primary peritoneal (HPMC) and immortalized pleural mesothelial cells (MeT-5A), and compared it to endothelial cells from umbilical vein (HUVEC) and cardiac capillaries (HCMEC).
Project description:Pleural fibrosis is defined as an excessive deposition of extracellular matrix that results in destruction of the normal pleural tissue architecture and compromised function. There is no effective medication for this disorder. Pleural mesothelial cells (PMCs/ Met-5A) play a key role in the process of pleural fibrosis. However, the detailed mechanisms are poorly understood. In our study, firstly SRSF6 protein has a major role in pleural fibrosis progression. To explore downstream of SRSF6, RNA sequencing was performed in Met-5A treated by bleomycin(0.2ug/ml) with SRSF6 siRNA or negtive control siRNA (siRNA NC). In conclusion, SRSF6 induced pleural fibrosis through a cluster pathway including SRSF6/WNT5A and SRSF6/SMAD1/5/9 signaling. SRSF6 is involved in pleural fibrosis, inhibition of SRSF6 is a novel strategy for treatment.
Project description:transcriptional profiling of makignant mesothelioma cell lines comparing control one immortalized mesothelial cell line, MeT-5A, and 2 primary normal mesothelial cultures collected from ascites of non-cancer patients, OV-M1 and GAS-M1
Project description:transcriptional profiling of makignant mesothelioma cell lines comparing control one immortalized mesothelial cell line, MeT-5A, and 2 primary normal mesothelial cultures collected from ascites of non-cancer patients, OV-M1 and GAS-M1 Two-condition experiment, mesothleioma cells vs. normal mesothelial cells
Project description:The objectives of the study were to examine the gene expression profile of human pleural mesothelial cells following infection with Streptococcus pneumoniae. The abstract is as follows: Streptococcus pneumoniae (Spn) is a major causative organism of empyema, an inflammatory condition occurring in the pleural sac. In this study, we used human and Spn cDNA microarrays to characterize the transcriptional responses occurring during initial contact between Spn and a human pleural mesothelial cell line (PMC) in vitro. Using stringent filtering criteria, 42 and 23 Spn genes were up-and down-regulated respectively. In particular, genes encoding factors potentially involved in metabolic processes and Spn adherence to eukaryotic cells were up-regulated e.g. glnQ, glnA, aliA, PsaB, LytB and nox. After Spn initial contact, 870 human genes were differentially regulated and the largest numbers of significant gene expression changes were found in canonical pathways for eukaryotic initiation factor 2 signaling (60 genes out of 171), oxidative phosphorylation (32/103), mitochondrial dysfunction (37/164), eIF4 and p70S6K signaling (28/142), mTOR signaling (27/182), NRF2-mediated oxidative stress response (20/177), epithelial adherens junction remodeling (11/66) and ubiquitination (22/254). The cellular response appeared to be directed towards host cell survival and defense. Spn did not activate NF-kB or phosphorylate p38 MAPK or induce cytokine production. Moreover, Spn infection of TNF-α pre-stimulated PMC inhibited production of IL-6 and IL-8 secretion by >50% (p<0.01). In summary, his descriptive study provides datasets and a platform for examining further the molecular mechanisms underlying the pathogenesis of empyema.
Project description:To investigate whether the EVs from cancer cell lines could change gene expression in mesothelial cells, the EVs from five types of cells (ES-2 cells, A2780 cells, SKOV3 cells, HOSE1 cells and HOSE2 cells) were added to MeT-5A cells (Fig. 2a). All three selected cancer cell lines expressed metastatic phenotypes in mouse model (Fig. 1c), and EVs from HOSE2 cell line, established together with HOSE1 cell line, was also set as control. Total mRNAs were extracted by MeT-5A cells treated with EVs, and then microarray analysis was performed.
Project description:To investigate whether exosomes from ovarian cancer cell lines could change lncRNA expression in mesothelial cells, exosomes from ovarian cancer cells (SKOV3 cells, A2780 cells) were added to MeT-5A cells, PBS treatment was set as blank control. Total RNAs of MeT-5A cells treated with exosomes were extracted, and then lncRNA sequencing was performed.
Project description:Establishment of immortalized human omental mesothelial cell lines (HOMCs) resulted in cloning three sublines (HOMC-B1, A4 and D4) with different morphologies. HOMC-B1 forms an epithelial-like monolayer. HOMC-A4 shows spindle-shaped morphology (storiform pattern). HOMC-D4 displayed an intermediate appearance. With the aim of exploring the key genes on decision of cellular morphology, gene expression of HOMC cell lines were analyzed along with conventional normal pleura-derived cell line, MeT-5A.
Project description:To determine the transcriptional program that imparts adhesion capacity to healthy mesothelial cells, we analyzed subtle gene expression changes by performing highly parallel single-cell RNA-seq genome-wide expression profiling of individual mesothelial cells exposed to stress (Extended Figure 6A) using the Drop-seq workflow (Pubmed ID 26000488). We individually sequenced >16,000 cells from Met-5A mesothelial cells at various time-points after exposure to a 15 min desiccation shock, as well as under control unstressed conditions.
