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C-Jun protein expression in vivo induces systemic fibrosis in mice

ABSTRACT: Time course analysis of c-Jun expression at 24h resulted in upregulation of a number of well-known fibrogenesis-associated factors.

ORGANISM(S): Mus musculus

PROVIDER: GSE84838 | GEO | 2016/07/26

SECONDARY ACCESSION(S): PRJNA335344

REPOSITORIES: GEO

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c-Jun protein expression in vivo induces systemic fibrosis in mice

Project description:Time course analysis of c-Jun expression at 24h resulted in upregulation of a number of well-known fibrogenesis-associated factors. We compared the global gene expression pattern of mouse whole bone marrow after c-Jun induction in vivo at 24h with no induction and applied to standard Affymetrix mouse arrays.

2016-07-26 | E-GEOD-84838 | biostudies-arrayexpress

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Project description:Serine/threonine kinase 40 (Stk40) was previously identified as a direct target gene of pluripotency-associated transcription factor Oct4 and its overexpression could facilitate differentiation of mouse embryonic stem cells (mESCs) towards the extraembryonic endoderm. Stk40-/- mice are lethal at the perinatal stage, displaying multiple organ failures. However, the molecular mechanisms underlying the physiological functions of Stk40 remain elusive. Here, we report that Stk40 ablation compromises the mesoderm differentiation from mESCs in vitro and in embryos. Mechanistically, Stk40 interacts with both mammalian constitutive photomorphogenic protein 1 (Cop1) and c-Jun, promoting degradation of c-Jun. Consequently, Stk40 knockout leads to c-Jun protein accumulation, which, in turn, might suppress the Wnt signaling activity and impair the mesoderm differentiation process. Overall, this study reveals that Stk40, together with Cop1, represent a novel axis for modulating c-Jun protein levels within an appropriate range during mesoderm differentiation from mESCs. Our finding provides new insight into the molecular mechanism regulating c-Jun protein stability and may have potential for managing related cellular disorders.

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Transcriptome analysis of JUN overexpressed or JUN inactivated fibroblasts

Project description:To examine the effects of phosphorylated JUN-mediated enhancers activation on gene expression, we conducted RNA-seq analysis in JUN wildtype (WT) or JUN inactive mutant (JUN AA) overexpressed MRC5 cells. The expression levels of genes associated with JUN-activated enhancers are significantly upregulated in JUN WT cells rather than in JUN AA cells. To quantify the effects of JUN inactivation on gene expression, we also performed RNA-seq analysis in JNKi-treated induced CAFs (iCAFs). We observed that JNKi significantly reduced expression levels of JUN-activated enhancers-associated genes.

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