Diabetic nephropathy streptozotocin db db
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE710 | GEO | 2004/01/20
SECONDARY ACCESSION(S): PRJNA87679
REPOSITORIES: GEO
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Project description:Diabetic nephropathy(DN) is a common diabetic microvascular complication, the underlying mechanisms involved in DN remain to be elucidated. We used microarrays to explore the global profile of gene expression for better understanding the molecular mechanism of diabetic nephropathy in type 2 diabetic db/db mice.
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Project description:Diabetic nephropathy(DN) is a common diabetic microvascular complication, Irbesartan is the first-line drug for clinical treatment of diabetic nephropathy, but its pharmacological mechanism and target are not yet fully clear. We used microarrays to explore the global profile of gene expression for better understanding the action mechanism of irbesartan in alleviating renal injuries of diabetic db/db mice
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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.
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Project description:Gene expression profiling in glomeruli from human kidneys with diabetic nephropathy Keywords = Diabetes Keywords = kidney Keywords = glomeruli Keywords: other
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Project description:The transcription factor c-Maf has been widely studied and has been reported to play a critical role in embryonic kidney development; however, the postnatal functions of c-Maf in adult kidneys remain unknown as c-Maf null C57BL/6J mice exhibit embryonic lethality. In this study, we investigated the role of c-Maf in adult mouse kidneys by comparing the phenotypes of tamoxifen (TAM)-inducible c-Maf knockout mice (c-Maf flox/flox; CAG-Cre-ERTM mice named “c-Maf ΔTAM”) with that of c-Maf flox/flox control mice, 10 days after TAM injection (TAM(10d)). In addition, we examined the effects of c-Maf deletion on diabetic conditions by injecting the mice with streptozotocin (STZ), 4 weeks before TAM injection. c-Maf ΔTAM mice displayed primary glycosuria caused by Sglt2 and Glut2 downregulation in the kidneys without diabetes, as well as morphological changes and life-threatening injuries in the kidneys on TAM(10d). Under diabetic conditions, c-Maf deletion promoted recovery from hyperglycemia and suppressed albuminuria and diabetic nephropathy by causing similar effects as did Sglt2 knockout and SGLT2 inhibitors. In addition to demonstrating the unique gene regulation of c-Maf, these findings highlight the renoprotective effects of c-Maf deficiency under diabetic conditions and suggest that c-Maf could be a novel therapeutic target gene for treating diabetic nephropathy.
2023-02-01 | GSE199916 | GEO
Project description:Murine models have been valuable instruments in defining the pathogenesis of diabetic nephropathy (DN), but they only partially recapitulate disease manifestations of human DN, limiting their utility . In order to define the molecular similarities and differences between human and murine DN, we performed a cross-species comparison of glomerular transcriptional networks. Glomerular gene expression was profiled in patients with early type 2 DN and in three mouse models (streptozotocin DBA/2 mice, db/db C57BLKS, and eNOS-deficient C57BLKS db/db mice). Species-specific transcriptional networks were generated and compared with a novel network-matching algorithm. Three shared, human-mouse cross-species glomerular transcriptional networks containing 143 (Human-STZ), 97 (Human- db/db), and 162 (Human- eNOS-/- db/db) gene nodes were generated. Shared nodes across all networks reflected established pathogenic mechanisms of diabetic complications, such as elements of JAK-STAT and VEGFR signaling pathways . In addition, novel pathways not formally associated with DN and cross-species gene nodes and pathways unique to each of the human-mouse networks were discovered. The human-mouse shared glomerular transcriptional networks will assist DN researchers in the selection of mouse models most relevant to the human disease process of interest. Moreover, they will allow identification of new pathways shared between mice and humans. We used microarrays to analyze the transcriptome of three different diabetic mouse models Glomerular RNA was extracted using the RNeasy Mini Kit and processed for hybridization on Affymetrix GeneChip Mouse Genome 430 2.0 microarrays.
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Project description:Epigenetic changes present in many physiological and pathological processes. The N6-methyladenosine (m6A) modification is the most common modification in eukaryotic mRNA. However, the role of m6A modification in diabetic nephropathy (DN) is still elusive. Here, the level of m6A modification was significantly upregulated in podocytes stimulated by high glucose (HG), which was caused by elevated levels of METTL3. The results were consistent in the streptozotocin (STZ)-induced experimental model of type 1 diabetes and db/db type 2 diabetes mice. Knocking out METTL3 significantly reduced the inflammation and apoptosis of HG-stimulated podocytes, while its overexpression significantly aggravated these responses. More importantly, silencing METTL3 both in type 1 and type 2 diabetic mice in vivo significantly reduced urinary albumin excretion and histopathological injury. Mechanistically, METTL3 modulated Notch signaling via the m6A modification of its target gene, TIMP2, and exerted pro-inflammatory and pro-apoptotic effects. Moreover, METTL3 enhanced the stability of TIMP2 in an insulin-like growth factor 2 mRNA binding protein 2 (IGF2BP2)-dependent manner. In summary, this study suggested that METTL3-mediated m6A modification is an important mechanism of podocyte injury in DN. Targeting m6A through the writer enzyme METTL3 is a potential approach for the treatment of DN.
2024-12-08 | GSE190436 | GEO
Project description:Diabetic nephropathy is a chronic complication of diabetes, presenting albuminuria at an early stage and leading to renal failure. Kidney is a complicated organ, which is responsible for body fluids control, acid-base balance, and removal of toxins. To better understand the progress of diabetic nephropathy, mice renal cortex of control mice, six-week db-/- (increased serum glucose without pathological changes in kidneys), and ten-week db-/- (with pathological changes in kidneys) were collected for single-cell sequencing analyses. A subgroup of glomerular endothelial cells with pro-angiogenetic features was identified in diabetic kidneys.
2023-10-27 | GSE206015 | GEO