Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

RNA-seq analysis of C. elegans CPEB homolog mutants.

ABSTRACT: Comparative transcriptomics study between C. elegans wild-type N2 and CPEB homolog mutants: fog-1, cpb-2, and cpb-3.

INSTRUMENT(S): Illumina HiSeq 2500

ORGANISM(S): Caenorhabditis elegans

SUBMITTER: Kapil Dev Singh

PROVIDER: E-MTAB-4720 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Differential regulation of germ line apoptosis and germ cell differentiation by CPEB family members in C. elegans.

Singh Kapil Dev KD Zheng Xue X Milstein Stuart S Keller Martin M Roschitzki Bernd B Grossmann Jonas J Hengartner Michael O MO

PloS one 20170731 7

Cytoplasmic polyadenylation element binding (CPEB) proteins are evolutionary conserved RNA-binding proteins that control mRNA polyadenylation and translation. Orthologs in humans and other vertebrates are mainly involved in oogenesis. This is also the case for the C. elegans CPEB family member CPB-3, whereas two further CPEB proteins (CPB-1 and FOG-1) are involved in spermatogenesis. Here we describe the characterisation of a new missense allele of cpb-3 and show that loss of cpb-3 function lead ...[more]

PMID: 28759574

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Project description:Cardiopulmonary bypass (CPB), the mechanical support required during the majority of cardiac surgeries, causes significant systemic inflammation and multi-organ dysfunction that is especially severe in neonatal patients. Currently, the limited understanding of the molecular mechanisms that underlie CPB-associated inflammation presents a significant barrier to the development of therapeutic interventions. To address this knowledge gap, we performed mRNA sequencing of total circulating leukocytes from neonatal patients undergoing CPB. The transcriptional signatures across 7 time points ranging from pre-CPB, during CPB, to 24 hours post-CPB were found to be dominated by myeloid cells, particularly monocytes. INTERLEUKIN-8 (IL8) and TUMOR NECROSIS FACTOR-α (TNFα) were two inflammatory cytokines specifically and robustly upregulated in the leukocytes from both CPB patients and piglets exposed to CPB. To delineate the mechanism how CPB activates cytokine production, we exposed THP-1 cells, a human monocyte cell line, in vitro to CPB-like conditions including artificial surfaces, high shear stress and cooling/rewarming. The in vitro CPB data recapitulated the in vivo CPB condition in that IL8 and TNFα were strongly upregulated. Shear stress was the major driver of cytokine expression as compared to the temperature or plastic exposure. Extracellular calcium influx was found essential for the shear-stress mediated upregulation of cytokines via the MEK/ERK/AP-1 and Calcineurin/NFAT pathways. After being exposed to CPB conditions, a subpopulation of THP-1 cells died by apoptosis and TNFα-mediated necroptosis, the latter form of which potentially contribute to the post-CPB tissue injuries. Together, our study is the first to elucidate the shear-stress modulated molecular mechanisms leading to systemic inflammation in pediatric CPB and the link between inflammation and organ damage. Calcium signaling pathways and TNFα signaling are novel targets for therapeutic development to improve clinical outcomes. To our knowledge, these are also the first data to implicate necroptosis in CPB and show that shear stress can activate necroptosis.

Dataset Information

RNA-seq analysis of C. elegans CPEB homolog mutants.

Publications

Differential regulation of germ line apoptosis and germ cell differentiation by CPEB family members in C. elegans.

Similar Datasets

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