Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA132031 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Transcriptome analysis of Advanced glycation end products treated ligament cells
| PRJNA275546 | ENA
Project description:Platelet-secreted microRNA-223 promotes endothelial cell apoptosis induced by advanced glycation end products via targeting the insulin-like growth factor 1 receptor
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Project description:Ossification of the posterior longitudinal ligament (OPLL) is formed by heterogeneous ossification of posterior longitudinal ligament. The patho-mechanism of OPLL is still largely unknown. Recently, disorders of metabolism are thought to be the center of many diseases such as OPLL. Advanced glycation end product (AGE) are accumulated in many extracellular matrixes such as ligament fibers, and it can functions as cellular signal through its receptor (RAGE), contributing to various events such as atherosclerosis or oxidative stress. However, its role in OPLL formation is not yet known. Therefore, we performed high-through-put RNA sequencing on primary posterior longitudinal ligament cells treated with different doses of AGEs (1µM, 5µM and negative control), with or without BMP2 (1µM).
2016-02-16 | GSE65952 | GEO
Project description:Ossification of the posterior longitudinal ligament (OPLL) is formed by heterogeneous ossification of posterior longitudinal ligament. The patho-mechanism of OPLL is still largely unknown. Recently, disorders of metabolism are thought to be the center of many diseases such as OPLL. Advanced glycation end product (AGE) are accumulated in many extracellular matrixes such as ligament fibers, and it can functions as cellular signal through its receptor (RAGE), contributing to various events such as atherosclerosis or oxidative stress. However, its role in OPLL formation is not yet known. Therefore, we performed high-through-put RNA sequencing on primary posterior longitudinal ligament cells treated with different doses of AGEs (1µM, 5µM and negative control), with or without BMP2 (1µM). mRNA profiles of Primary human posterior longitudinal ligament cells stimulated with various stimuli (Control, 1µM AGE-BSA, 5µM AGE-BSA, 1µM AGE-BSA with BMP2, 5µM AGE-BSA with BMP2) were generated by deep sequencing on Ion Proton
2016-02-16 | E-GEOD-65952 | biostudies-arrayexpress
Project description:Advanced glycation end-products (AGEs) accumulate in brain tissue with as we age, co-localizing with amyloid β and tau in the brains of elderly and Alzheimer’s disease patients. However, the link between increased AGE levels, aging, and neurodegeneration remains unclear. To explore the effect and mechanism of AGEs on the brain, we developed a neurovascular (NV) model that reflects features of an aged brain by integrating an AGE-anchored matrix. Notably, we discovered that targeting AGE and its receptor could attenuate AGE-mediated neurodysfunction through the histone-modifying enzyme, KMT2A, in neurons within an aged NV model.
2025-10-31 | GSE278799 | GEO
Project description:Podocyte dysfunction is considered as the main contributor to the development and progression of diabetic kidney disease(DKD).High glucose(HG)or advanced glycation end products (AGEs) can lead to podocyte dysfunction.To explore the the molecular mechanism of podocyte dysfunction, we screened the mRNA expression profiles of podocytes treated with HG(50mmol/L)and AGEs(400µg/mL) through transcriptomics.
2024-12-31 | GSE236426 | GEO
Project description:Prostate cancer, a leading cause of male cancer mortality, poses major therapeutic hurdles due to its immunosuppressive tumor microenvironment (TME). We link MYC amplification and PTEN deletion to metastatic prostate adenocarcinoma and identify a specific population of tumor-associated non-classical monocytes (staNC-Mo, CD11b+Ly6cLowCD14HiCD43LowCX3CR1Low) as key mediators of immune suppression. MYC overexpression with Pten loss induces mitochondrial stress, triggering tumor-cell apoptosis and HSP60 release. The HSP60/TLR4 signaling activates staNC-Mo to secrete TNF-α, stimulating endothelial G-CSF production and driving staNC-Mo differentiation in bone marrow and spleen. CD14-dependent phagocytosis of apoptotic tumor cells drives staNC-Mo senescence and TGF-β1 secretion. TGF-β1 activates PI3K/AKT signaling in tumor cells, inducing CXCL5 secretion and reinforcing staNC-Mo recrutiment. Senescent staNC-Mo also release IL-18, suppressing innate and adaptive immunity. Targeting Ly6c, CD14, CXCL5-CXCR2, TLR4, or IL-18 reduces staNC-Mo accumulation, relieves TME immunosuppression, and inhibits tumor progression, suggesting therapeutic strategies for advanced prostate cancer.
2026-09-02 | GSE345439 | GEO
Project description:Glycation, or non-enzymatic glycosylation, has recently attracted increasing interest in the context of its impact on aging. Advanced glycation end products (AGEs) contribute to various age-related pathological conditions such as inflammation, fibrosis, stem cell aging, etc. However, the molecular mechanisms underlying the glycation-induced disruption of cell-matrix interactions during cellular senescence are not fully understood. The aim of this study was to investigate transcriptomic changes in young and senescent dermal fibroblasts (HdFbs) cultivated in post-glycated 3D collagen type I matrices after 10 and 17 days. Our findings indicate that the D-ribose-mediated glycation increases the accumulation of fluorescent AGEs and the stiffness of the matrices in a dose-dependent manner. The transcriptome alterations encompassed the modulation of age-related genes and signaling pathways, including the activation of genes related to senescence-associated secretory phenotype (SASP) in young cells. Notably, the alterations in the transcriptome profiles due to glycation were more pronounced (in terms of both the number of genes and their fold changes) on day 10 of cultivation compared to day 17 in both passages.
2025-06-04 | GSE293225 | GEO