Gene expresion analysis among young mouse embryos, aging mouse embryos and aging mouse embryos suppressed their CXCL5-CXCR2 signaling.
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ABSTRACT:
PROVIDER: PRJNA649904 | ENA |
REPOSITORIES: ENA
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Project description:CXCL5-CXCR2 signailing is known as senescence-associated secretory phenotype (SASP) factor to promote cellular senescense in diverse cells. We identified CXCL5 as a SASP factor in human and mouse embryos and suppression of CXCL5-CXCR2 signaling during embryo culture improved pregnancy success in aging mice. Here, we perfomed microarray analysis using mouse blastocysts for comparing gene expression pattarns among young mouse embryos, aging mouse embryos and aging mouse embryos suppressed their CXCL5-CXCR2 signaling. As a results, gene expression pattern of CXCL5-CXCR2 signaling-suppressed aging blastocysts was closer to that of the young blastocysts as compared with aging blastocysts. In addition, cell proliferation-related pathways, such as “PI3K signaling pathway” and “RAS signaling pathway” were significantly enriched in CXCL5-suppressed blastocysts.
2020-10-07 | GSE155477 | GEO
Project description:The pregnancy rate of women decreases with age due to declining quality of oocytes and embryos. However, there is no established method to improve pregnancy rate in aging women. Here, we performed microarray analysis for detecting candidate genes affected the quality of aging embryos. Based on microarray analysis using young and aging human embryos at the same morphological grade, 820 genes showed > 5-fold change in aging human blastocysts. Among these genes, C-X-C motif chemokine 5 (CXCL5), one of SASP factors, showed 7.2-fold increases in aging human blastocysts. These findings indicate CXCL5, one of senescence-associated secretory phenotype (SASP) factors, partially responsible for the decline in embryo implantation potentia.
2020-10-07 | GSE155476 | GEO
Project description:CXCL5, a strong neutrophil-chemoattractant, has been reportet to be expressed in different cancer entities with diverse outcomes in disease progression. Contradictory outcome in disease progression in different tumor entities might be explained by a tumor type specific expression pattern of chemokines, chemokine receptors and growth factors that act in concert with CXCL5. This study evaluates the impact of CXCL5 expression on the tumor mircoenvironment in a syngeneic mouse melanoma model.
2018-07-19 | GSE101104 | GEO
Project description:Cerebral small vessel disease and brain white matter injury are worsened by cardiovascular risk factors including obesity. Molecular pathways in cerebral endothelial cells activated by chronic cerebrovascular risk factors alter cell-cell signaling, blocking endogenous and post-ischemic white matter repair. Using cell-specific translating ribosome affinity purification(RiboTag) in white matter endothelia and oligodendrocyte progenitor cells (OPCs), we identify a coordinated interleukin-chemokine signaling cascade within the oligovascular niche of subcortical white matter that is triggered by diet-induced obesity (DIO).DIO induces IL-17B signaling that acts on the cerebral endothelia through IL-17Rb to increase both circulating and local endothelial expression of CXCL5. In white matter endothelia, CXCL5 promotes the association of OPCs with the vasculature and triggers OPC gene expression programs regulating cell migration through chemokine signaling. Targeted blockade of IL-17B reduced vessel-associated OPCs by reducing endothelial CXCL5 expression. In multiple human cohorts, blood levels of CXCL5 function as a diagnostic and prognostic biomarker of vascular cognitive impairment.
2022-11-11 | GSE217354 | GEO
Project description:Cerebral small vessel disease and brain white matter injury are worsened by cardiovascular risk factors including obesity. Molecular pathways in cerebral endothelial cells activated by chronic cerebrovascular risk factors alter cell-cell signaling, blocking endogenous and post-ischemic white matter repair. Using cell-specific translating ribosome affinity purification(RiboTag) in white matter endothelia and oligodendrocyte progenitor cells (OPCs), we identify a coordinated interleukin-chemokine signaling cascade within the oligovascular niche of subcortical white matter that is triggered by diet-induced obesity (DIO).DIO induces IL-17B signaling that acts on the cerebral endothelia through IL-17Rb to increase both circulating and local endothelial expression of CXCL5. In white matter endothelia, CXCL5 promotes the association of OPCs with the vasculature and triggers OPC gene expression programs regulating cell migration through chemokine signaling. Targeted blockade of IL-17B reduced vessel-associated OPCs by reducing endothelial CXCL5 expression. In multiple human cohorts, blood levels of CXCL5 function as a diagnostic and prognostic biomarker of vascular cognitive impairment.
2022-11-11 | GSE217355 | GEO
Project description:BACKGROUND: CXCR1/2 inhibitors are being implemented with immunotherapies in PDAC clinical trials. CXCL ligands are a family of cytokines responsible for stimulating these receptors; while typically secreted by activated immune cells, fibroblasts, and even adipocytes, they are also secreted by immune-evasive cancer cells. CXCL ligand release is known to occur in response to inflammatory stimuli, whether pathogenic (bacterial) or endogenous (obesity). Obesity has been linked to poor patient outcome and altered anti-tumor immunity in pancreatic cancer. Importantly, adipose-derived cytokines and chemokines have been implicated as potential drivers of tumor cell immune evasion; cumulatively these findings suggest that targeting CXC ligands may be beneficial in the context of obesity. METHODS: RNA-sequencing of human PDAC cell lines was used to assess differential influences of adipose conditioned media on the cancer cell transcriptome. In addition, the adipose-induced secretome of PDAC cells was validated with ELISA for induced CXCL5 secretion. Human tissue data from CPTAC was used to correlate IL-1β and TNF expression with both CXCL5 mRNA and protein levels. CRISPR-Cas9 was used to knock out CXCL5 from a murine PDAC cell line in order to assess orthotopic tumor studies in syngeneic, diet-induced obese mice. Flow cytometry was used to compare the immune profiles between tumors. Mice were monitored for differences in tumor size at endpoint in combination with Anti-PD-1 immune checkpoint blockade therapy. RESULTS: Human adipose conditioned media (hAT-CM) stimulates CXCL5 secretion from PDAC cells via either IL-1β or TNF; neutralization of both is required to significantly block release of CXCL5 from tumor cells. Ablation of CXCL5 from tumors promoted an enriched immune phenotype with an unanticipatedly increased number of exhausted CD8 T cells. Application of anti-PD-1 treatment to control tumors failed to alter tumor growth, yet treatment of CXCL5 deficient tumors showed response by significantly diminished tumor mass. CONCLUSIONS: In summary, our findings show that both TNF and IL-1β can stimulate CXCL5 release from PDAC cells in vitro, which correlates with expression in patient data. CXCL5 depletion in vivo alone is sufficient to promote T cell infiltration into tumors, increasing efficacy of checkpoint blockade inhibition and alleviating tumor burden.
2024-08-31 | GSE274713 | GEO
Project description:Comparison of Mycobacterium tuberculosis infection in WT mice strain C57BL/6 (WT) and the CXCL5 knockout (KO)
2014-09-02 | GSE43337 | GEO
Project description:Adipose tissue affects metabolic-related diseases as it consists of various types of cells that are involved in fat metabolism and adipokine release. CXC ligand 5 (CXCL5) is a member of the CXC chemokine family and is highly expressed by macrophages in white adipose tissue (WAT). In this study, we generated and investigated the function of Cxcl5 in knockout (KO) mouse. Cxcl5 KO mouse was generated using CRISPR/Cas9. The KO male mice didn’t show significant phenotype difference in normal condition. However, proteomic analysis revealed that many proteins are enriched in the process of fatty acid beta-oxidation and mitochondrial localization in iWAT of Cxcl5 KO mice. Cxcl5 KO mouse showed rather decreased proteins and transcripts expression associated with thermogenesis including uncoupled protein 1 (UCP1), a well-known thermogenic gene, and increased expressions associated with inflammation. The increase of Ucp1 expression in cold conditions was significantly retarded in Cxcl5 KO mice. The expression of transcription factors involved in thermogenesis including peroxisome proliferator-activated receptor gamma coactivator 1-alpha (Pgc1α) was not properly increased in Cxcl5 KO under cold challenge and its mimic conditions. CXCL5 treatment increased the expression of transcription factors for Ucp1 and Ucp1 itself. Collectively, our data shows that Ucp1 expression is induced in adipocyte by CXCL5 secreted by β-Adrenergic stimulation in M1 macrophages. Our data indicates that CXCL5 has a crucial role in regulating energy metabolism, particularly in cold exposure. These results strongly suggest that targeting CXCL5 could be a therapeutic aim for people with a disorder of energy metabolism.
2022-07-14 | PXD027291 | JPOST Repository
Project description:Analysis of proteome changes during mouse brain aging
| MSV000082968 | MassIVE
Project description:Comparison of Mycobacterium tuberculosis infection in WT mice strain C57BL/6 (WTM-BM-^]) and the CXCL5 knockout (KO) Two color arrays with dye swaps, RNA harvested at day 0 (d00, no infection) and day 21 (d21); 5 mice per experimental group. RNA from each experimental group was pooled. The e0, e8, e9 and eX are internal experimental run/labels of equivalent biological replications of the experiments.
2014-09-02 | E-GEOD-43337 | biostudies-arrayexpress