Project description:Here we characterized and compared differential gene expression from diabetic and normoglycemic NOD mice and from aged and young-adults Balb/c mice. Total RNA from NOD diabetic (3 weeks with glicemia over 500mg/dl) and normoglycemic NOD mice from the same age was used. To compare the effects of aging in genomic expression, total RNA from young-adult Balb/c (9 weeks old) and middle-aged Balb/c (47 weeks old) were used.
Project description:Here we characterized and compared differential gene expression from diabetic and normoglycemic NOD mice and from aged and young-adults Balb/c mice.
Project description:We investigated the gene expression profiles of RNA isolated from kidney glomeruli from aged, 25 week old type-2 diabetic (db/db) and non-diabetic mice.
Project description:Increased amounts of the mitochondrial apolipoprotein O /MIC26 were found in diabetic patients along with lipid accumulation in murine liver upon MIC26 expression. MIC26 is a MICOS complex constituent present in the mitochondrial inner membrane. Here, we employed a proteomics analysis approach in WT and MIC26 knockout HepG2 cellular models in normoglycemic and hyperglycemic conditions.
Project description:The goal of this study is to determine whether PRMT2 plays a causal role in the impairment of atherosclerosis regression in diabetes. We examined the consequence of deleting PRMT2 in myeloid cells during the regression of atherosclerosis in normal and diabetic mice. We found significant impairment of atherosclerosis regression under normoglycemic conditions in mice lacking PRMT2 (Prmt2-/-) in myeloid cells that mimic the decrease in regression of atherosclerosis in WT mice under diabetic conditions. This was associated with increased plaque macrophage retention. PRMT2-deficient plaque CD68+ cells under normoglycemic conditions showed increased expression of genes involved in cytokine signaling and inflammation compared to WT cells by RNA seq. Thus, the loss of PRMT2 is causally linked to impaired atherosclerosis regression.
Project description:We investigated the gene expression profiles of RNA isolated from kidney glomeruli and renal tubules from aged, 24 week old type-2 diabetic (db/db) and non-diabetic mice
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.
Project description:Transcriptome analysis was carried out to characterise the different responses of diabetic and non-diabetic WT and p75KO mice to ischemia C57BL/6J-p75NTR-/- (p75KO) and p75NTR+/+ (WT) littermates were bred starting from breeding pairs. Six to seven week old male p75KO and WT mice were made diabetic using streptozotocin (STZ, 40 mg/kg in 0.1mol/l citrate buffer pH4.5 i.p. per day for 5 days or left normoglycemic by STZ buffer injections. One or three months after diabetes induction, anesthetized mice underwent unilateral hindlimb ischemia by permanent ligation and electro-coagulation of the proximal end of femoral arteries. At the same time, full thickness wounds were created in the thigh dorsal skin of both legs using a sterile 5-mm-wide biopsy punch. Samples for gene expression analysis were taken from the wounds three days later.
Project description:We investigated the gene expression profiles of RNA isolated from kidney glomeruli from aged, 25 week old type-2 diabetic (db/db) and non-diabetic mice. In order to investigate the consequences of hyperglycemia on the pathogenesis and progression of diabetic nephropathy Kidney glomeruli from 3 diabetic and 3 non-diabetic, control mice were isolated and RNA purified for RNA-Seq analysis on the Illumina HiSeq 2000. The goal of the project was to generate comprehensive list of noncoding RNA genes differentially regulated between the two conditions in order to identify novel targets for further study.
