Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA236377 | ENA |
REPOSITORIES: ENA
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Project description:Little is known about the function of induced pluripotent stem cell-derived endothelial cells (iPSC-ECs) generated from diabetics, as this could potentially limit subsequent therapeutic use in this patient population. Here, we demonstrate that iPSC-ECs derived from diet-induced obesity (DIO) mice exhibit evidence of endothelial dysfunction. We also observed that mice receiving intramuscular (IM) injections of DIO iPSC-ECs had significantly decreased reperfusion following hindlimb ischemia compared to mice administered with iPSC-ECs from control mice. Hindlimb sections revealed increased muscle atrophy and presence of inflammatory cells in mice receiving iPSC-ECs from DIO mice. When pravastatin was administered to mice receiving DIO iPSC-ECs, a significant increase in reperfusion was observed, which was blunted by co-administration of L-NAME. This study is the first to provide evidence that iPSC-ECs from pre-diabetic mice exhibit signs of endothelial function, and suggest that pravastatin administration may be needed for diabetic patients receiving autologous iPSC-ECs therapy in the clinic. Four samples were analyzed, two from the healthy (control) group and two from the diet-induced obesity group
2014-01-25 | E-GEOD-54387 | biostudies-arrayexpress
Project description:Little is known about the function of induced pluripotent stem cell-derived endothelial cells (iPSC-ECs) generated from diabetics, as this could potentially limit subsequent therapeutic use in this patient population. Here, we demonstrate that iPSC-ECs derived from diet-induced obesity (DIO) mice exhibit evidence of endothelial dysfunction. We also observed that mice receiving intramuscular (IM) injections of DIO iPSC-ECs had significantly decreased reperfusion following hindlimb ischemia compared to mice administered with iPSC-ECs from control mice. Hindlimb sections revealed increased muscle atrophy and presence of inflammatory cells in mice receiving iPSC-ECs from DIO mice. When pravastatin was administered to mice receiving DIO iPSC-ECs, a significant increase in reperfusion was observed, which was blunted by co-administration of L-NAME. This study is the first to provide evidence that iPSC-ECs from pre-diabetic mice exhibit signs of endothelial function, and suggest that pravastatin administration may be needed for diabetic patients receiving autologous iPSC-ECs therapy in the clinic.
2014-01-25 | GSE54387 | GEO
Project description:We sequenced the transcriptomes of seven samples of hypothalamic neurons dervied from pluripotent stem cells taken from healthy patients; five samples of hypothalamic neurons derived from pluripotent stem cells of constitutionally obese donors; five samples of sectioned hypothalami from post-mortem dissection of brains, and two samples for motor neurons derived from pluripotent stem cells of healthy donors in order to assess the similarity of our iPSC-derived cells against those of sectioned brains and to identify possible transcriptional disfunction which might underlie extreme, inherited obesity.
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Project description:Induced pluripotent stem cells (iPSCs) were generated from peripheral blood cells of a patient with ID and differentiated into neurons. Label-free phosphoproteomics was used to assess the phosphorylation of proteins in neurons derived from both patients and healthy controls.
2024-10-23 | PXD057079 |
Project description:Obesity is a health problem characterized by large expansion of adipose tissue. During this expansion, genotoxic stressors can be accumulated and negatively affect the Mesenchymal Stem Cells (MSCs) of adipose tissue. Due to the oxidative stress generated by these genotoxic stressors, senescence phenotype might be observed in adipose tissue MSCs. Senescent MSCs lose their proliferations and differentiation properties and secrete senescence-associated molecules to their niche thus triggering senescence for the rest of the tissue. Accumulation of senescent cells in adipose tissue results in decreased tissue regeneration and functional impairment not only in the close vicinity but also in the other tissues. Here we hypothesized that declined tissue regeneration might be associated with loss of stemness in MSCs population. We analyzed the expression of several stemness genes in adipose tissue MSCs of high-fat diet and normal diet mice models. Since the MSCs population covers a small percentage of the pluripotent stem cells, a role in proliferation and tissue regeneration, we measured the percentage of these cells via TRA-1-60 surface antigen. Additionally, by conducting a shotgun proteomic approach using LC-MS/MS, whole cell proteome of the adipose tissue MSCs of high-fat diet and normal diet mice were analyzed and identified proteins were evaluated via Gene Ontology and PPI network analysis. MSCs of obese mice showed senescent phenotype and altered cell cycle distribution due to a hostile environment with oxidative stress in adipose tissue where they reside. Additionally, the number of pluripotent markers expressing cells declined in the MSC population of the high-fat diet mice. Gene expression analysis evidenced the loss of stemness with a decrease in the expression of stemness-associated genes. Of the proteomic comparison of the normal and the high-fat diet group, MSCs revealed that stemness-associated molecules were decreased while inflammation and senescence-associated phenotypes emerged in obese mice MSCs. Our results showed us that the MSCs of adipose tissue may lose their stemness properties due to obesity-associated stress conditions.
2024-10-17 | PXD050811 | Pride
Project description:Obesity and its co-morbidities including type 2 diabetes are increasing at epidemic rates in the U.S. and worldwide. Brown adipose tissue (BAT) is a potential therapeutic to combat obesity and type 2 diabetes. Increasing BAT mass by transplantation improves metabolic health in rodents, but its clinical translation remains a challenge. Here, we investigated if transplantation of 2-4 million differentiated brown pre-adipocytes from mouse BAT stromal fraction (SVF) or human pluripotent stem cells (hPSCs) could improve metabolic health. Transplantation of differentiated brown pre-adipocytes, termed ‘committed pre-adipocytes’ from BAT SVF from mice or derived from hPSCs improves glucose homeostasis and insulin sensitivity in recipient mice under conditions of diet-induced obesity, and this improvement is mediated through the collaborative actions of the liver transcriptome, tissue AKT signaling and FGF21. These data demonstrate that transplantation of a small number of brown adipocytes has significant long-term translational and therapeutic potential to improve glucose metabolism.
2023-12-13 | GSE250078 | GEO
Project description:This dataset contains proteomic data from mice with high or low weight gain in response to a high fat diet. Both host and microbial proteins are present. In the supplemental, there are also tables and supplementary files that can be used for replicating the bioinformatic analysis.
Abstract:
Consumption of refined high-fat, low-fiber diets promotes development of obesity and its associated consequences. While genetics play an important role in dictating susceptibility to such obesogenic diets, mice with nearly uniform genetics exhibit marked heterogeneity in their extent of obesity in response to such diets. This suggests non-genetic determinants play a role in diet-induced obesity. Hence, we sought to identify parameters that predict, and/or correlate with, development of obesity in response to an obesogenic diet. We assayed behavior, metabolic parameters, inflammatory markers/cytokines, microbiota composition, and the fecal metaproteome, in a cohort of mice (n=50) prior to, and the 8 weeks following, administration of an obesogenic high-fat low-fiber diet. Neither behavioral testing nor quantitation of inflammatory markers broadly predicted severity of diet-induced obesity. Although, the small subset of mice that exhibited basal elevations in serum IL-6 (n=5) were among the more obese mice in the cohort. While fecal microbiota composition changed markedly in response to the obesogenic diet, it lacked the ability to predict which mice were relative prone or resistant to obesity. In contrast, fecal metaproteome analysis revealed functional and taxonomic differences among the proteins associated with proneness to obesity. Targeted interrogation of microbiota composition data successfully validated the taxonomic differences seen in the metaproteome. While future work will be needed to determine the breadth of applicability of these associations to other cohorts of animals and humans, this study nonetheless highlights the potential power of gut microbial proteins to predict and perhaps impact development of obesity.
2019-06-04 | MSV000083891 | MassIVE