Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Controlled Nutrient Delivery to Pancreatic Islets Using Polydopamine-Coated Mesoporous Silica Nanoparticles

ABSTRACT: In the present study, we designed a nanoscale platform for the sustained and controlled delivery of nutrients to pancreatic islets-upon transplantation. Our platform consists of a mesoporous silica nanoparticle (MSNP), loaded with glutamine (G), an essential amino acid required for islet survival and function, and capped with polydopamine (PD). To control the release of glutamine, various concentrations (0.5 - 2 mg/mL) of PD and incubation times (0.5 – 2 h) with MSNPs were investigated in terms of pharmacological properties and biological functions. After extensive testing, PD-G-MSNPs made using PD coating of 0.5 mg/mL incubated for 0.5 h resulted in the optimal platform to maintain the islet viability and functionality in vitro. Following syngeneic renal sub-capsule islet transplantation in STZ-diabetic mice, PD-G-MSNPs improved the engraftment of pancreatic islets as well as their function, resulting in re-establishment of glycemic control. Collectively, our data shows that PD-G-MSNPs can support transplanted islets by providing them with a controlled and sustained supply of nutrients.

ORGANISM(S): Mus musculus

PROVIDER: GSE247020 | GEO | 2023/12/04

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Transcription profiling of mouse pancreatic islets from wild type and DcR3 transgenic mice to investigate primary non-function (PNF) in islet transplantation

Project description:The islet primary non-function (PNF) is a serious problem in islet transplantation. In this study, we investigated whether DcR3-secreting transgenic (Tg) islets could reduce PNF. We generated transgenic mice expressing human DcR3. The transgenically expressed DcR3 protected islets from IFN-gama plus IL-1beta, or TNF-alpha plus IL-1beta-induced dysfunction and apoptosis in vitro. The Tg islets presented significantly reduced PNF after transplantation. <br><br> Three independent batches of islet isolation were carried out. For each batch, islets were obtained from 4 Tg and 4 WT mice, and pooled respectively. The pooled islets (Tg or WT) were then divided into 4 groups: 2 were cultured in the presence of IFN-gamma (0.5 ug/ml) plus IL-1beta (0.5 ng/ml) with 1 harvested at 24 h and 1 harvested at 48 h; 2 were cultured in the presence of TNF-alpha (100 ng/ml) plus IL-1beta (0.5 ng/ml) with 1 harvested at 24 h and 1 harvested at 48 h. Each treatment employed 3 chips using RNA from 3 different batches of islet isolation. For each treatment, genes with a mean signal strength difference above 2-fold between Tg and WT islets were selected for reverse PCR confirmation.

2009-08-15 | E-MEXP-2306 | biostudies-arrayexpress

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

Successful transplantation of islets into inguinal subcutaneous white adipose tissue

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

Paired box 6 gene delivery preserves beta cells and improves islet transplantation efficacy

Project description:Loss of pancreatic beta cells is the central feature of all forms of diabetes. Current therapies fail to halt the declined beta cell mass. Thus, strategies to preserve beta cells are imperatively needed. In this study, we identified paired box 6 (PAX6) as a critical regulator of beta cell survival. Under diabetic conditions, the human beta cell line EndoC-bH1, db/db mouse and human islets displayed dampened insulin and incretin signalings and reduced beta cell survival, which were alleviated by PAX6 overexpression. Adeno-associated virus (AAV)-mediated PAX6 overexpression in beta cells of streptozotocin-induced diabetic mice and db/db mice led to a sustained maintenance of glucose homeostasis. AAV-PAX6 transduction in human islets reduced islet graft loss and improved glycemic control after transplantation into immunodeficient diabetic mice. Our study highlights a previously unappreciated role for PAX6 in beta cell survival and raises the possibility that ex vivo PAX6 gene transfer into islets prior to transplantation might enhance islet graft function and transplantation outcome.

2023-10-13 | GSE242338 | GEO

Expression data from the transplanted mouse islets into hyperglycemic and normoglycemic mice at 6 hours post-transplantation

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

Transcription profiling of pancreatic islet implanted transgenic (expressing survivini) in mice

Project description:Transgenic mice were generated that expressed the inhibitor of apoptosis and mitotic regulator survivin in pancreatic islet beta cells. Control non-transgenic or transgenic islets were then used in a model of islet transplantation in diabetic recipient mice and tested for their ability to correct hyperglycemia and allow long-term engraftment of tranplanted islets in vivo. Control or transgenic islets were analyzed by chip microarray for potential transcriptional changes associated with transgenic expression of survivin, in vivo.

2006-01-16 | E-MEXP-536 | biostudies-arrayexpress

Interruption of Hepatic Glucagon Signaling Reveals a Hepatic-α-Islet Cell Axis Where L-Glutamine Stimulates α-Cell Proliferation

Project description:Decreasing glucagon action lowers blood glucose and may be a useful therapeutic approach for diabetes. However, interrupted glucagon signaling in mice leads to hyperglucagonemia and α-cell hyperplasia. We show using islet transplantation, mouse and zebrafish models, an in vitro islet culture assay that a hepatic-derived, circulating factor in mice with interrupted glucagon signaling stimulates α-cell proliferation, which was dependent on mTOR signaling and the FoxP transcription factors. α-cells of transplanted human islets also proliferated in response to this signal in mice. A combination of liver transcriptomics and serum fractionation with proteomics/metabolomics found changes in hepatic gene expression relating to amino acid catabolism predicting the observed increase in serum amino acid levels. Amino acid concentrations that mimicked the levels in mice with interrupted glucagon signaling, specifically L-glutamine, stimulated α-cell proliferation. These results indicate a hepatic-α-islet cell axis where glucagon regulates serum amino acid availability and L-glutamine regulates α-cell proliferation via mTOR-dependent nutrient sensing.

2017-03-31 | GSE89035 | GEO

Expression data from the transplanted mouse islets into hyperglycemic and normoglycemic mice at 6 hours post-transplantation

2014-04-18 | GSE55764 | GEO

Gene expression from human pancreatic islet

Project description:Expression profiling of cell cycle genes in human pancreatic islets with and without type 2 diabetes Islets from cadaver donors were provided by the Nordic Islet Transplantation Programme (www.nordicislets.org), Uppsala University. The microarrays were performed using GeneChipM-BM-. Human Gene 1.0 ST whole transcript according to Affymetrix standard protocol.

2013-03-15 | E-GEOD-44035 | biostudies-arrayexpress

Transplant tissue specfic exosome platform for noninvasive monitoring of immunologic rejection [miRNA]

Project description:In transplantation, there is a critical need for non-invasive biomarker platforms for monitoring immunologic rejection. We hypothesized that transplanted tissues release donor specific exosomes into recipient circulation/ bodily fluids, and that the quantitation and profiling of their intra-exosomal cargoes would constitute a novel biomarker platform for monitoring rejection. We tested this hypothesis in a human into mouse xenogeneic islet transplant model, and validated the concept in clinical settings of islet and renal transplantation. In the xenogeneic model, islet transplant exosomes in recipient blood were quantified over long-term follow-up using anti-human leukocyte antigen (HLA) antibody that is only expressed on human islets (p=1.6x10-14). Transplant islet exosomes were purified using anti-HLA antibody conjugated beads and their cargoes contained bona fide islet endocrine hormone markers insulin, glucagon, and somatostatin. Rejection led to significant decrease in transplant islet exosome signal (p=4x10-15), along with distinct changes in its microRNA and proteomic profiles prior to appearance of hyperglycemia. In the clinical settings of islet (n=5) and renal (n=5) transplantation, donor exosomes with respective tissue specificity for islet β cells and renal epithelial cells were reliably characterized in recipient plasma over follow-up (up to 5 years; p=0.0001). Collectively, these findings demonstrate the biomarker potential of transplant exosome characterization for providing a non-invasive window into the conditional state of the transplant tissue.

2016-10-18 | GSE88845 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data