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Transcriptomic alterations in ferroptotic murine embryonic fibroblasts

ABSTRACT: Transcriptomic alterations in ferroptotic murine embryonic fibroblasts

PROVIDER: PRJNA543663 | ENA |

REPOSITORIES: ENA

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Transcriptomic alterations in ferroptotic murine embryonic fibroblasts

Project description:Alterations of metabolic and biological processes occur in ferroptotic cells. We analyzed transcriptional responses of murine embryonic fibroblasts (MEFs) exposed to a ferroptosis inducer erastin. We found that a set of genes related to protection against oxidative stress was induced upon ferroptosis and Bach1 promoted ferroptosis by repressing a set of these genes involved in synthesis of glutathione or metabolism of intracellular labile iron. Our findings suggests that ferroptosis is programmed at transcriptional level and Bach1 works as a controller in setting a threshold of ferroptosis.

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Project description:We provide an original multi-stage approach identifying a gene signature to assess the fibroblast polarization. Prototypic polarizations (inflammatory/fibrotic) were induced by seeded mouse embryonic fibroblasts (MEFs) with TNFα or TGFß1, respectively. The transcriptomic and proteomic profiles were obtained by RNA microarray and LC/MS-MS. Gene Ontology and pathways analysis were performed among the differentially expressed genes (DEGs) and proteins (DEPs). Balb/c mice underwent daily intradermal injections of HOCl (or PBS) as an experimental murine model of inflammation-mediated fibrosis in a time-dependent manner. As results, 1,456 and 2,215 DEGs, and 289 and 233 DEPs were respectively found in MEFs in response to TNFα or TGFß1, respectively. Among the most significant pathways, we combined 26 representative genes to encompass the proinflammatory and profibrotic polarizations of fibroblasts. Based on principal component analysis, this signature deciphered baseline state, proinflammatory polarization, and profibrotic polarization as accurately as did RNA microarray and LC/MS-MS. Then, we assessed the gene signature on dermal fibroblasts isolated from the experimental murine model. We observed a proinflammatory polarization at day 7, and a mixture of a proinflammatory and profibrotic polarizations at day 42 in line with histological findings. Our approach provides a small-size and convenient gene signature to assess murine fibroblast polarization.

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