MicroRNA microarray profiling in the livers of control db/+ and diabetic db/db mice
Ontology highlight
ABSTRACT: Analysis revealed a set of 13 microRNAs to be significantly altered between livers of control db/+ and diabetic db/db mice. Of these, miR-34a, miR-107, miR-378, miR-378*, miR-31, miR-31*, miR-151-5p, miR-676, miR-22, miR-93, let-7b were up-regulated and let-7e and miR-227 were down-regulated. A total of 670 predicted targets for these altered miRNAs were extracted from PicTar and TargetScan and functional characterisation mapped these targets to several biological processess related to varied metabolic pathways. The Wnt signaling pathway that has been shown to be linked to diabetes emerged as the most prominent pathway from these sets of target genes.
Project description:MiR-132 is one of the most upregulated miRNAs in human skin wounds at the inflammatory phase of healing. MiR-132 inhibits inflammation but promotes growth of epidermal keratinocytes, indicating that it may facilitate the inflammatory-proliferative phase transition during wound repair. Following this line of research, here we evaluated the therapeutic potential of miR-132 in chronic wound using mouse in vivo wound model. We performed a global transcriptome analysis of skin wounds of leptin receptor-deficient (db/db) mice treated with miR-132 or control mimics. Db/db mouse has been used as a type 2 diabetic model with impaired wound healing capacity.
Project description:Transcriptional profiling of mouse white adipose tissues. The objective of this study is to explore gene expression profiles of obese adipose tissue by DNA microarray data analysis. Male db/db (BKS.Cg-m+/+ Lepr db/J, 6 weeks old) and db/+ (BKS.Cg-Dock7m +/+ Lepr db/J, 6 weeks old) mice were used in this experiment.
Project description:This program addresses the molecular basis of beta-cell failure associated with the development of type 2 diabetes in the db/db mice. Specifically, which genes are differentially expressed in pancreatic islets of the db/db mice compared to the control db/+ mice?
Project description:This program addresses the molecular basis of beta-cell failure associated with the development of type 2 diabetes in the db/db mice. Specifically, which genes are differentially expressed in pancreatic islets of the db/db mice compared to the control db/+ mice? The db/db mice islets profiling data was analyzed by identifying genes that were up- and down-regulated at selected p value and fold change in the islets of db/db mice compared to the corresponding db/+ controls.
Project description:Gene expression of liver tissue from db/db untreated (6x replicates) and db/db treated with 5mg/kg of 3c7.v44 mAb (6x replicates). Anti-GCGR antibody treatment in db/db mice: fig 2b in Solloway et al.
Project description:Purpose: RNA seq analysis were to compare and contrast the gene expression profile involved in the dedifferentiation of db/db islets in type 2 diabetes Methods: Islets of wild type, db/+ and db/db were purified using perfusion from 12 week old mice and RNA were isolated. Islated RNA were used in RNA seq to understand the expression pattern Results: Using an optimized data analysis workflow, we mapped about 10 million sequence reads per sample to the mouse genome (build mm9) and identified 16,014 transcripts WT, db/+ and db/db mice islets with TopHat workflow. Hierarchical clustering of differentially expressed genes uncovered there role in type 2 diabetes. Data analysis with TopHat workflows revealed a significant overlap yet provided complementary insights in transcriptome profiling. Conclusions: We characterised and identified genes involved in dedifferentiation of islets.
Project description:This program addresses the gene signature associated with the development of type 2 diabetes in the db/db mice. Specifically, which genes are differentially expressed in adipose tissue of the db/db mice compared to the control db/+ mice?