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Whole Transcriptome Sequencing (mRNA-seq) of cultured pulmonary primary endothelial cells treated with or without H2O2

ABSTRACT: ROS once released from myeloid cells is quickly converted into H2O2 in lungs. We performed RNAseq of cultured pulmonary primary endothelial cells treated with or without H2O2. Pathway enrichment analysis revealed that some of the signaling pathways that are altered by H2O2 are related to AKT signaling. AKT signaling has a protective role in a murine model of ALI by preventing capillary leakage. Moreover, H2O2 stimulates AKT activation in endothelial cells to strengthen vessel barrier integrity

ORGANISM(S): Mus musculus

PROVIDER: GSE134373 | GEO | 2020/07/10

REPOSITORIES: GEO

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Atf1-mediated active gene response to H2O2 challenge.

Project description:Here we present the study on ChIP-chip mapping of the genomic binding sites for Sty1, Atf1, and the Atf1's binding partner Pcr1; the genome-wide transcriptional profiling of the atf1 and pcr1 strains in response to H2O2; and the phenotypic assessment of ~90 Atf1/Pcr1-bound or unbound genes for growth fitness under H2O2 conditions. ChIP-chip analysis shows that Atf1 and Pcr1 binding sites are overlapped in the genome and constitutively present before H2O2 stress. On the other hand, Sty1 recruitment primarily occurs at the Atf1/Pcr1 binding sites and is induced by H2O2. We found that Atf1/Pcr1 is clearly responsible for the high-level transcriptional response to H2O2. Furthermore, phenotypic assessment indicates that among the H2O2-induced genes, Atf1/Pcr1-bound genes exhibit a higher likelihood of functional requirement for growth fitness under the stress condition than the Atf1/Pcr1-unbound genes do. Notably, we found that the Atf1/Pcr1-bound genes regardless of their responsiveness to H2O2 show a high probability of requirement for growth fitness. .

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