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High-resolution whole-genome DNA methylation revealed unique signatures of painful diabetic neuropathy

ABSTRACT: High-resolution whole-genome DNA methylation revealed unique signatures of painful diabetic neuropathy

PROVIDER: PRJNA1208965 | ENA |

REPOSITORIES: ENA

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High-resolution whole-genome DNA methylation revealed unique signatures of painful diabetic neuropathy

Project description:This work describes the DNA methylation signature and identifies genes associated with neuropathic pain in type 2 diabetes mellitus. Genome-wide methylation data for 315 DNA (WB) samples were generated using Illumina Infinium Methylation EPIC v1.0 BeadChip. Four different selection criteria were used to identify promising pain-related genes. The findings revealed significant differences in methylation patterns between painful and painless diabetic neuropathy and identified a set of individual CpG sites of unique candidate genes associated with the painful phenotype. Several of these genes, including GCH1, MYT1L and MED16, have been previously linked to pain-related phenotypes or diabetes. Through pathway enrichment analysis, we demonstrated that specific epigenetic signatures could contribute to the complex phenotype of diabetic neuropathy and cluster analyses highlighted significant epigenetic dissimilarities between painful and painless phenotypes. Our results uncovered epigenetic differences between painful and painless diabetic neuropathy patients and identified targeted genes linked to neuropathic pain through DNA methylation mechanisms. This approach holds promise for investigating other chronic pain conditions, such as secondary chronic pain from cancer treatment, thoracic surgery, and various transplant settings.

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Expression data from the dorsal root ganglia during streptozotocin-induced painful diabetic neuropathy in rats

Project description:FK1706 potentiated nerve growth factor-induced neurite outgrowth, putatively mediated via FKBP-52 and the Ras/Raf/MAPK signaling pathway. It also improved mechanical allodynia accompanied by the recovery of intraepidermal nerve fiber density in a painful diabetic neuropathy in rats. We analyzed gene expression of the dorsal root ganglia together with measurement of mechanical allodynia in diabetic rats to try to capture the global fingerprint of changes in gene expression associated with FK1706 administration and also to elucidate the putative mechanisms of its neurotrophic activity in vivo. Normal, STZ-treated controls, and STZ + FK1706 groups were used to evaluate gene expression analysis. Dorsal root ganglia from L4 to L6 were collected at the day after 1, 2, and 3 weeks of FK1706 administration, were immediately immersed in RNAlater reagent, and stored as instructed before RNA extraction. Equal amounts of total RNA from five rats were collected for each group.

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Project description:Painful diabetic peripheral neuropathy (PDPN) is a common complication of diabetes mellitus (DM). As one of the most disturbing symptoms, mechanical allodynia (MA) in PDPN remains largely unexplored. This dataset contains single-cell RNA sequencing results from rat dorsal root ganglion (DRG). The goal of this experiment was to investigate the transcriptional changes of distinct cell types in the DRG along MA development.

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Microbial-derived Hyodeoxycholic Acid Ameliorates Painful Diabetic Neuropathy by Modulating Dorsal Root Ganglion TLR4-Mediated Neuroinflammation Signaling Pathway

Project description:Microbial-derived Hyodeoxycholic Acid Ameliorates Painful Diabetic Neuropathy by Modulating Dorsal Root Ganglion TLR4-Mediated Neuroinflammation Signaling Pathway

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Transcription profiling of diabetic neuropathy in dorsal root ganglia from streptozotocin-diabetic male wistar rats over the first 8 weeks of diabetes

Project description:A study of diabetic neuropathy in dorsal root ganglia from streptozotocin-diabetic male wistar rats over the first 8 weeks of diabetes

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Dorsal root ganglion single-cell RNA-seq dataset of painful diabetic peripheral neuropathy rat, diabeitc rats, and health rats

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Single-cell transcriptome analysis reveals distinct cell populations in dorsal root ganglia and their potential roles in diabetic peripheral neuropathy

Project description:Diabetic peripheral neuropathy (DPN) is the most common form of neuropathy, and have considerable morbidity, which occurs in approximately 50% of diabetic patients. Here, we performed scRNA-seq technology using 10× Genomics sequencing on DRG tissues isolated from control and DPN rats, to identify the cell type composition of DRG, and to reveal the roles of different cell types in mediating DPN.

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Project description:Diabetic peripheral neuropathy (DPN) is a common complication of diabetes mellitus (DM). It is not diagnosed or managed properly in the majority of patients, because its pathogenesis remains controversial. In this study, using microarray-based genome-wide expression analyses, we sought to identify both common and distinct mechanisms underlying the pathogenesis of DM and DPN. The results demonstrated that down-regulation of the neurotrophin-MAPK signaling pathway may be the major mechanism of DPN pathogenesis, thus providing a potential approach for DPN treatment.

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Sarm1 knockout prevents type 1 diabetic bone disease in females independent of neuropathy

Project description:Diabetic patients have a high risk of developing skeletal diseases accompanied by diabetic peripheral neuropathy (DPN). In this study, we isolated the role of DPN in skeletal disease with global and conditional knockout models of sterile-α and TIR-motif-containing protein-1 (Sarm1). SARM1, an NADase highly expressed in the nervous system, regulates axon degeneration upon a range of insults, including DPN. Global knockout of Sarm1 prevented DPN, but not skeletal disease, in male mice with type 1 diabetes (T1D). Female wild type mice also developed diabetic bone disease, but without DPN. Unexpectedly, global Sarm1 knockout completely protected female mice from T1D-associated bone suppression and skeletal fragility despite comparable muscle atrophy and hyperglycemia. Global Sarm1 knockout rescued bone health through sustained osteoblast function with abrogation of local oxidative stress responses. This was independent of the neural actions of SARM1, as beneficial effects on bone were lost with neural conditional Sarm1 knockout. This study demonstrates that the onset of skeletal disease occurs rapidly in both male and female mice with T1D completely independent of DPN. In addition, this reveals that clinical SARM1 inhibitors, currently being developed for treatment of neuropathy, may also have benefits for diabetic bone through actions outside of the nervous system.

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