Expression of long non‑coding RNA and mRNA in the hippocampus of mice with type 2 diabetes

Abstract

Long non-coding RNAs (lncRNAs) serve key roles in cell growth, development and various diseases associated with the central nervous system. However, differential expression profiles of lncRNAs in type 2 diabetes have not been reported. The present study aimed to analyze the expression pattern of lncRNA-mRNA in a type 2 diabetic mouse model using microarray analysis. The mouse model of type 2 diabetes was established and the total RNAs were extracted from the hippocampus of the mice used in the present study. The total RNAs were then examined by the GeeDom human lncRNA + mRNA V4.0 expression profile and analyzed through comparing Gene Ontology (GO) enrichment analysis and signal pathway analysis with the Kyoto Encyclopedia of Genes and Genomes (KEGG) database. There were statistically significant differences between the expression of IncRNAs and mRNA in the healthy mice and that of the diabetic mice. In the diabetic mice, 130 different lncRNAs were expressed with 126 significantly upregulated and 4 significantly downregulated and 49 different mRNAs were detected with 45 significantly upregulated and 4 downregulated. GO analysis indicated that the mRNAs that are affected are involved in transport, cell adhesion, ion transport and metabolic processes. KEGG and Reactome enrichment analysis indicated that mRNAs impact on cholinergic synapses, nuclear factor-kB pathway, Toll like receptor 4 cascade and zinc transporter are correlated with cognitive dysfunction in type 2 diabetes. A dynamic lncRNA-mRNA network was constructed containing 123 lncRNAs and 48 mRNAs, which can elucidate the interaction between lncRNA and mRNA. Overall, this is the first study to indicate that lncRNAs are differentially expressed in the type 2 diabetic mice.

The Differential Expression of Long Noncoding RNAs in Type 2 Diabetes Mellitus and Latent Autoimmune Diabetes in Adults

“…In fact, most are enriched in the cytoplasm, while some are partially enriched in the nucleus or concurrently enriched in the nucleus and cytoplasm [8]. Initially, lncRNAs were viewed as "junk genes" that lack coding capacity [9]; however, they were discovered to be important in many human diseases such as diabetes, cancer, neurodegenerative diseases, cardiovascular diseases, and autoimmune diseases, such as T1DM [10,11]. LncRNAs can interact with DNA, proteins, mRNAs, miRNAs, siRNAs, and other antisense RNAs via chromatin modification [8,12], thereby acting as a bait or promoter of transcription factors [4], DNA methylation, histone modification, and genomic imprinting [13] and promoting or inhibiting translation; these interactions are involved in gene expression and regulation [14].…”

Clinical impact of type 2 diabetes mellitus on outcomes after one-lung ventilation during thoracic surgery: a retrospective cohort study

“…A study (16) showed that the incidence of bacterial infection in DM patients was 1.2 times higher than that if healthy volunteers, and the mortality of DM patients whose blood sugar was effectively controlled was more than 2.0 times higher than that of healthy volunteers. High blood sugar level would activate various protein kinase C isoforms, which regulate the expression of nitric oxide, endothelin, nuclear transcription factor-kB, and plasminogen activator inhibitor (PAI) to affect the release of cytokines and insulin (17,18). This study also showed that thoracic patients with T2DM were accompanied by higher preoperative WBC count, suggesting activated inflammation.…”

2-Dodecyl-6-Methoxycyclohexa-2,5-Diene-1,4-Dione Ameliorates Diabetic Cognitive Impairment Through Inhibiting Hif3α and Apoptosis

“…To date, only a few mRNAs and lncRNAs have been reported to be dysregulated and functionally characterized in diabetic cognitive impairment. Microarray provides a comprehensive assessment of expressed probes and allows identification of mRNAs and lncRNAs with diagnostic, prognostic, and functional potential in diabetic cognitive impairment ( Ci et al, 2018 ; Santiago et al, 2019 ). To find the potential target genes of DMDD and cell signaling associated with diabetic cognitive impairment treatment, we test the gene expression profile in the hippocampi of db/db mice by RNA microarray.…”