Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA240907 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:insulin treatment protects islets from the initial rapid loss that is usually observed after transplantation and positively affects the outcome of islet transplantation in Akita mice. To study the molecular mechanism underlying the improved islet survival, expression profile analyses was performed to analyze the differences between the grafts transplanted into hyperglycemic and normoglycemic mice at 6 hours post-transplantation Cells were harvested at grafts for RNA extraction and hybridization on Affymetrix microarrays. We performed gene expression profiles of the transplanted mouse islets into hyperglycemic and normoglycemic mice at 6 hours post-transplantation
2014-04-18 | E-GEOD-55764 | biostudies-arrayexpress
Project description:insulin treatment protects islets from the initial rapid loss that is usually observed after transplantation and positively affects the outcome of islet transplantation in Akita mice. To study the molecular mechanism underlying the improved islet survival, expression profile analyses was performed to analyze the differences between the grafts transplanted into hyperglycemic and normoglycemic mice at 6 hours post-transplantation
2014-04-18 | GSE55764 | GEO
Project description:From the past reports, we hypothesized that spleen is an ideal site for inducing regeneration of transplanted islets, and leading to reduce the required number of islets for ameliorating the hyperglycemia of diabetic recipients in mice. In order to confirm this hypothesis, we performed 25 islets transplantation into spleen (SP25); it was not enough number to ameliorate the hyperglycemia of recipient mice, with 100 islets transplantation into beneath the kidney capsule (KC100) to maintain recipients' blood glucose normoglycemic temporary. All recipient mice (n=11) became normoglycemic after receiving SP25 with KC100. On 240 days after transplantation, we performed nephrectomy for removing islet grafts in the kidney. After nephrectomy, 8 of 11 mice remained normoglycemic, and 3 of 11 mice' non-fasting blood glucose levels were maintained around 300 mg/dL. On 290 days after transplantation (50 days after nephrectomy), all recipient mice received splenectomy to remove islet grafts in the spleen. All mice became hyperglycemic after splenectomy, indicating that intra-splenic islet grafts maintained the blood glucose levels of diabetic recipient mice. In order to investigate the gene expression associated with islets engraftment in the spleen, microarray studies were performed in comparison of the Tlx-1 (Hox11) related gene expression profiles of Sample 1, Sample 2 and Sample 3.
2017-03-01 | GSE84512 | GEO
Project description:To assess the effect of transplantation on human islet signature, we transplanted 500-800 human iselts under the kidney capsule of diabetic mice. The mice were rendered diabetic with allowan. The transplanted islets were collected after 30 days, and compared to non-trasnplanted islets.
2025-04-03 | PXD044502 | Pride
Project description:Two healthy iPSC lines were differentiated into ECs. iPSC-ECs were then treated under normoglycemic (5.5mM glucose) or hyperglycemic (33mM glucose) conditions with and without MDL-28170 (2.5 uM) for 72 hours.
2019-02-15 | GSE123699 | GEO
Project description:Islet transplantation is an attractive treatment for patients with insulin-dependent diabetes mellitus, and currently the liver is the favored transplantation site. However, an alternative site is desirable because of the low efficiency of hepatic transplantation, requiring 2-3 donors for a single recipient, and because the transplanted islets cannot be accessed or retrieved. Here we describe a novel site for islet transplantation, the inguinal subcutaneous white adipose tissue. In this site, transplanted islets are engrafted as clusters and function to reverse diabetes in mice. Importantly, transplanted islets can be visualized by CT and are easily retrievable, and allograft rejection is preventable by blockade of co-stimulatory signals. Of much interest, the efficiency of islet transplantation is superior to the liver, with increased mass of transplanted β cells. Furthermore, transplanted human islets function to reverse diabetes in immunodeficient mice. Thus, this adipose tissue site may be ideal for clinical islet transplantation.
2018-03-01 | GSE95595 | GEO
Project description:Objective: The loss of insulin-secreting β-cells, ultimately characterizing most diabetes forms, demands the development of cell replacement therapies. The common endpoint for all ex vivo strategies is transplantation into diabetic patients. However, the effects of hyperglycemia environment on the transplanted cells were not yet properly assessed. Thus, the main goal of this study was to characterize global effect of brief and prolonged in vivo hyperglycemia exposure on the cell fate acquisition and maintenance of transplanted human pancreatic progenitors. Methods: To rigorously study the effect of hyperglycemia, in vitro differentiated human induced pluripotent stem cells (hiPSC)-derived pancreatic progenitors were xenotransplanted in normoglycemic and diabetic NSG RIP-DTR mice. The transplants were retrieved after one-week or one-month exposure to overt hyperglycemia and analyzed by large-scale microscopy or global proteomics. For this study we pioneer the use of the NSG RIP-DTR system in the transplantation of hiPSC, making use of its highly reproducible specific and absolute β-cell ablation property in the absence of inflammation or other organ toxicity. Results: Here we show for the first time that besides the presence of an induced oxidative stress signature, the cell fate and proteome landscape response to hyperglycemia was different, involving largely different mechanisms, according to the period spent in the hyperglycemic environment. Surprisingly, brief hyperglycemia exposure increased the bihormonal cell number by impeding the activity of specific islet lineage determinants. Moreover it activated antioxidant and inflammation protection mechanisms signatures in the transplanted cells. In contrast, the prolonged exposure was characterized by decreased numbers of hormone+ cells, low/absent detoxification signature, augmented production of oxygen reactive species and increased apoptosis. Conclusion: Hyperglycemia exposure induced distinct, period-dependent, negative effects on xenotransplanted human pancreatic progenitor, affecting their energy homeostasis, cell fate acquisition and survival.
2020-02-12 | PXD015071 | Pride
Project description:This study explores these differences by comparing the proteomes of proximal tubules and serum from normoglycemic (NG), pre-transplant T2DM, and PTDM patients one-year post-kidney transplantation.
2025-05-26 | PXD054961 | Pride
Project description:This study explores these differences by comparing the proteomes of proximal tubules and serum from normoglycemic (NG), pre-transplant T2DM, and PTDM patients one-year post-kidney transplantation.
2025-05-26 | PXD054937 | Pride
Project description:The intricate aetiology of type 1 diabetes mellitus (T1DM) implicating a detrimental cross talk between immune cells and insulin producing b-cells leading to their destruction has stumped the development of effective disease modifying therapies. The discovery that the pharmacological activation of LRH-1/NR5A2 can revert hyperglycemia in pre-clinical mouse models of T1DM by attenuating the autoimmune attack coupled to b-cell survival/regeneration, prompt us to investigate whether LRH-1/NR5A2-mediated immune tolerization could be achieved in individuals with T1DM and improve islet survival and function subsequent to xenotransplantation. We found that LRH-1/NR5A2 activation using the agonist BL001 blunted the pro-inflammatory genetic signature and cytokine secretome of both monocyte-derived macrophages (MDM1) and mature dendritic cells (mDCs) from individuals with T1DM. Mechanistically, mitohormesis was induced in MDM1 restricting pro-inflammation propagation while mitochondria turnover was increased in mDCs assisting transit towards a tolerogenic phenotype. BL001 treatment also increased T-regulatory cells within the T-cell subpopulation. BL001-treated MDM1, mDCs or T-cells impeded T-effector cell expansion. Engraftment and function of human islets transplanted into hyperglycemic immunocompetent mice was enhanced by BL001 treatment leading to improved glycemia. Collectively, LRH-1/NR5A2 agonism fosters a coordinated re-programming of T1DM immune cells from a pro- to an anti-inflammatory/tolerizing phenotype empowering them to repress cytotoxic T-cell proliferation and facilitates islet engraftment and function after transplantation. Our finding demonstrate the feasibility of re-establishing human immune tolerance within a pro-inflammatory environment, rather than suppression, opening an unprecedent pharmacological therapeutic venue for T1DM
2025-04-09 | PXD053517 | Pride