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A role for miR-4734 in conditional suppression of ER stress-associated pro-inflammatory responses [starved vs control HFF]

ABSTRACT: A role for miR-4734 in conditional suppression of ER stress-associated pro-inflammatory responses [starved vs control HFF]

PROVIDER: PRJNA887801 | ENA |

REPOSITORIES: ENA

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A role for miR-4734 in conditional suppression of ER stress-associated pro-inflammatory responses [starved vs control HFF]

Project description:Prolonged metabolic stress can lead to severe pathologies. In metabolically challenged primary fibroblasts, we assigned a novel role for the poorly characterized miR-4734 in restricting ATF4 and IRE1-mediated upregulation of a set of pro-inflammatory cytokines and endoplasmic reticulum (ER) stress-associated genes. Conversely, inhibition of this miRNA augmented the expression of those genes. Mechanistically, miR-4734 was found to restrict the expression of NFKBIZ, that is required for optimal expression of the pro-inflammatory genes and whose mRNA is targeted directly by miR-4734. Concordantly, overexpression of NFKBIZ compromised the effects of miR-4734, underscoring the importance of this direct targeting. As the effects of this miR-4734 were evident under stress, but not under basal conditions, it may be considered as a therapeutic agent.

2023-10-10 | GSE214961 | GEO

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Project description:ER stress underlies numerous severe pathologies. We have metabolically perturbed normal fibroblasts in order to study the biological roles of microRNAs (miRs) under mild and extended ER stress. We now report that miR-4488 quenches inflammation-associated gene expression in such metabolically perturbed cells. Furthermore, we define miR-4488 as a non-canonical miRNA derived from the expansion segment ES7L of the 28S ribosomal RNA. Generation of miR-4488 requires Dicer, but not Drosha. Moreover, its generation involves the autophagy-lysosome route and is inhibited when this pathway is blocked, thus unveiling an anti-inflammatory role for lysosomes engaged at the onset of stress. Mechanistically, miR-4488 suppresses the expression of NFKB2 and RELB, whose mRNAs specifically associate with miR-4488 exclusively upon stress. This selectivity suggests that miR-4488 may have promise for treating mild ER stress-associated diseases.

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