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Single cell sequencing datasets of tibial nerves from diabetic neuropathy (DPN) patients and traumatic limb amputation (TLA) patients.

ABSTRACT: To understand the cellular diversity and alterations in the pathogenesis of diabetic neuropathy (DPN), weenrolled 4 DPN patients, 3 traumatic limb amputation (TLA) patients at the Department of Orthopedic Surgery of Shanghai Sixth People’s Hospital, Shanghai, China.

ORGANISM(S): Homo sapiens

PROVIDER: GSE266026 | GEO | 2024/12/18

REPOSITORIES: GEO

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The expression of mRNA and lncRNA in peripheral blood mononuclear cells (PBMCs) of diabetes mellitus, diabetic retinopathy (DR), diabetic peripheral neuropathy (DPN) and diabetic nephropathy (DN) patients

Project description:DR, DPN and DN are common complications in diabetes, and the differentially expressed mRNAs and lncRNAs in these diabetic complications may help to identify the molecular markers for the onset and progression of diseases. In our study, high-throughput sequencing technique was used to analyze the expression profile of mRNA and lncRNA in the peripheral blood of health control, T2DM, DR, DPN and DN patients, in order to determine the differentially expressed transcriptomic profiles changes in diabetic complications and identify the shared and specific biological signaling pathways related to DR, DPN and DN.

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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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| S-EPMC4391274 | biostudies-literature

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