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Reduced insulin/IGF1 signaling prevents immune aging via ZIP-10/bZIP–mediated feedforward loop

ABSTRACT: Reduced insulin/IGF1 signaling prevents immune aging via ZIP-10/bZIP–mediated feedforward loop

PROVIDER: PRJNA1023268 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26259907_1.fastq.gz	Fastqsanger.gz
	SRR26259907_2.fastq.gz	Fastqsanger.gz
	SRR26259908_1.fastq.gz	Fastqsanger.gz
	SRR26259908_2.fastq.gz	Fastqsanger.gz
	SRR26259909_1.fastq.gz	Fastqsanger.gz

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Reduced insulin/IGF1 signaling prevents immune aging via ZIP-10/bZIP–mediated feedforward loop

Project description:A hallmark of aging is immunosenescence, a decline in immune functions, which appeared to be inevitable in living organisms, includingCaenorhabditis elegans. Here, we show that genetic inhibition of the DAF-2/insulin/IGF-1 receptor drastically enhances immunocompetence in old age inC. elegans. We demonstrate that longevity-promoting DAF-16/FOXO and heat-shock transcription factor 1 (HSF-1) increase immunocompetence in olddaf-2(−)animals. In contrast, p38 mitogen-activated protein kinase 1 (PMK-1), a key determinant of immunity, is only partially required for this rejuvenated immunity. The up-regulation of DAF-16/FOXO and HSF-1 decreases the expression of thezip-10/bZIP transcription factor, which in turn down-regulates INS-7, an agonistic insulin-like peptide, resulting in further reduction of insulin/IGF-1 signaling (IIS). Thus, reduced IIS prevents immune aging via the up-regulation of anti-aging transcription factors that modulate an endocrine insulin-like peptide through a feedforward mechanism. Because many functions of IIS are conserved across phyla, our study may lead to the development of strategies against immune aging in humans.

2023-10-04 | GSE244494 | GEO

Reduced insulin/IGF1 signaling prevents immune aging via ZIP-10/bZIP-mediated feedforward loop.

Project description:A hallmark of aging is immunosenescence, a decline in immune functions, which appeared to be inevitable in living organisms, including Caenorhabditis elegans. Here, we show that genetic inhibition of the DAF-2/insulin/IGF-1 receptor drastically enhances immunocompetence in old age in C. elegans. We demonstrate that longevity-promoting DAF-16/FOXO and heat-shock transcription factor 1 (HSF-1) increase immunocompetence in old daf-2(-) animals. In contrast, p38 mitogen-activated protein kinase 1 (PMK-1), a key determinant of immunity, is only partially required for this rejuvenated immunity. The up-regulation of DAF-16/FOXO and HSF-1 decreases the expression of the zip-10/bZIP transcription factor, which in turn down-regulates INS-7, an agonistic insulin-like peptide, resulting in further reduction of insulin/IGF-1 signaling (IIS). Thus, reduced IIS prevents immune aging via the up-regulation of anti-aging transcription factors that modulate an endocrine insulin-like peptide through a feedforward mechanism. Because many functions of IIS are conserved across phyla, our study may lead to the development of strategies against immune aging in humans.

| S-EPMC7941181 | biostudies-literature

Expression data from E18.5 Igf1 -/- (homozygous mutant) and Igf1+/+ (normal wild type control) mouse lungs

Project description:Insight into the role of Insulin-like Growth Factor (IGF) in development of lungs has come from the study of genetically modified mice. IGF1 is a key factor during lung development. IGF1 deficiency in the neonatal mouse causes respiratory failure collapsed alveoli and altered alveolar septa. To further characterize IGF1 function during lung development we analyzed Igf1-/- mouse prenatal lungs in a C57Bl/6 genetic background. Mutant lungs showed disproportional hypoplasia, disorganized extracellular matrix and dilated alveolar capillaries. IGF1 target genes during lung maturation were identified by analyzing RNA differential expression in Igf1-/- lungs using microarrays. Lungs from E18.5 were isolated from both Igf1+/+ wild type and Igf1-/- null mice and pooled to obtain RNA. Heterozygous male and female with a genetic background C57BL/6J were mated to obtain embryos at embrionic (E) stage 18.5 days post coitum (E18.5). 3 biological replicates per genotype.

2014-03-31 | E-GEOD-17157 | biostudies-arrayexpress

Targeting p16-induced Senescence Prevents Cigarette Smoke-Induced Emphysema by Promoting IGF1/Akt1 Signaling in mice

Project description:Increased IGF1 signaling in p16 -/- lungs

2019-06-27 | GSE133380 | GEO

Expression data from E18.5 Igf1 -/- (homozygous mutant) and Igf1+/+ (normal wild type control) mouse lungs

2014-03-31 | GSE17157 | GEO

Generating IGF1 signatures in human melanoma cell lines by activation of IGF1 or ihibition of IGF1R

Project description:To generate IGF1 signatures in human melanoma cell lines. Recombinant human IGF1 (rhIGF1) was added to WM35, known to be responsive to rhIGF1, whereas constitutive IGF1 signaling in Mel-624 was abrogated by siRNA directed against the IGF1 receptor (siIGF1R). Experiments were performed in triplicate in normoxia (O2 concentration, 21%) and hypoxia (1% O2), because hypoxia has been suspected to play an adverse role in melanoma. After generating GEP data, we created signatures of genes significantly (p ≤0.0001, q ≤0.05) and consistently upregulated in rhIGF1-treated WM35 cells, or similarly downregulated in siIGF1R-treated Mel-624 cells, as compared to control cells at the same O2 concentration.

2018-01-01 | GSE59343 | GEO

Identify genes regulated by zip-2 in absence and presence of P. aeruginosa PA14 infection at 4h

Project description:Very little is known about how animals discriminate pathogens from innocuous microbes. To address this question, we examined infection-response gene induction in the nematode Caenorhabditis elegans. We focused on genes that are induced in C. elegans by infection with the bacterial pathogen Pseudomonas aeruginosa, but are not induced by an isogenic attenuated gacA mutant. Most of these genes are induced independently of known immunity pathways. We generated a GFP reporter for one of these genes, infection response gene 1 (irg-1), which is induced strongly by wild-type P. aeruginosa strain PA14, but not by other C. elegans pathogens or by other wild-type P. aeruginosa strains that are weakly pathogenic to C. elegans. To identify components of the pathway that induces irg-1 in response to infection, we performed an RNA interference screen of C. elegans transcription factors. This screen identified zip-2, a bZIP transcription factor that is required for inducing irg-1, as well as several other genes, and is important for defense against infection by P. aeruginosa. These data indicate that zip-2 is part of a specialized pathogen response pathway that is induced by virulent strains of P. aeruginosa and provides defense against this pathogen. Analysis of differential gene expression in adult N2 C. elegans treated with L4440 control RNAi or zip-2 RNAi, either uninfected (feeding on E. coli) or infected with P. aeruginosa PA14; samples were analyzed after 4 hours of infection

2013-08-30 | E-GEOD-50513 | biostudies-arrayexpress

Insulin and IGF1 receptor function in murine podocytes

Project description:Project in which conditionally immortalised mouse podocytes had either their insulin, IGF1 or both receptors knocked down. 72 hours post receptor knock-down total proteomics was performed on 40 samples.

2024-04-04 | PXD051018 | Pride

ERa DNA Binding Profiles of IGF1 and ICI182,780 treated mouse uterus from manuscript: Role of ERα in Mediating Female Uterine Transcriptional Responses to IGF1

Project description:Estrogen (E2) signaling through its nuclear receptor, estrogen receptor α (ERα) increases insulin-like growth factor 1 (IGF1) in the rodent uterus, which then initiates further signals via the IGF1 receptor (IGF1R). Directly administering IGF1 results in similar biological and transcriptional uterine responses. Our studies using global ERα-null mice demonstrated a loss of uterine biological responses of the uterus to E2 or IGF1 treatment, while maintaining transcriptional responses to IGF1. To address this discrepancy in the need for uterine ERα in mediating the IGF1 transcriptional vs. growth responses, we assessed the IGF1 transcriptional responses in PgrCre+Esr1f/f (called ERαUtcKO) mice, which selectively lack ERα in progesterone receptor (PGR) expressing cells, including all uterine cells, while maintaining ERα expression in other tissues and cells that do not express Pgr. Additionally, we profiled IGF1-induced ERα binding sites in uterine chromatin using ChIP-seq. Herein, we explore the transcriptional and molecular signaling that underlies our findings to refine our understanding of uterine IGF1 signaling and identify ERα-mediated and ERα-independent uterine transcriptional responses. Defining these mechanisms in vivo in whole tissue and animal contexts provides details of nuclear receptor mediated mechanisms that impact biological systems and have potential applicability to reproductive processes of humans, livestock and wildlife.

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Differential expression analysis of wildtype and zip-3(gk3164) mutant with next generation sequencing

Project description:ZIP-3 has been shown to repress the mitochondrial-UPR genes and immune response during P. aeruginosa infection. To identify genes repressed by ZIP-3, we compared transcript profiles from wildtype and zip-3(gk3164) worms raised on P. aeruginosa or E. coli.

2019-01-30 | GSE111325 | GEO

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