Nerve action potential amplitude, a robust marker of diabetic peripheral neuropathy

Monlun, Marie; Hugo, M; Blanco, Laurence; Mohammedi, Kamel; Ahdab, Rechdi; Alexandre, L.; Poirot-Mazeres, Stéphane; Rajaobelina, Kalina; Rigalleau, Vincent

doi:10.1111/dme.13690

Diabet. Med.

2018

DOI: 10.1111/dme.13690

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Nerve action potential amplitude, a robust marker of diabetic peripheral neuropathy

Marie Monlun¹,

M Hugo²,

Laurence Blanco³

et al.

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2022

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“…Advanced glycation end products (AGEs) have been proven to be correlated with the development of diabetic complications [24,25]. Intensive studies have demonstrated that the formation of AGEs may play a role in the pathogenesis of diseases, such as impaired wound healing and diabetic neuropathy, and in diabetic retinopathy [26][27][28]. AGEs have been used to establish a cell model for the study of DFU and diabetic mesangium [29,30].…”

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Overexpression of miR-146a promotes cell proliferation and migration in a model of diabetic foot ulcers by regulating the AKAP12 axis

2022

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In the current study, we aimed to study the effect of miR-146a on proliferation and migration in an in vitro diabetic foot ulcer (DFU) model by targeting A-kinase-anchoring protein 12 (AKAP12). An in vitro DFU model was initially established using HaCaT cells derived from human keratinocytes and induced by advanced glycation end products (AGEs). The effects of overexpression of miR-146a on proliferation and migration ability were analysed. The expression levels of miR-146a and AKAP12 were measured by quantitative real-time polymerase chain reaction (qRT-PCR), and AKAP12, hypoxia-inducible factor-1α (HIF-1α), Wnt3a and β-catenin protein levels were measured by western blotting. The cell proliferation ability was measured by MTT, and the migration ability was analysed by a cell scratch assay. The binding between miR-146a and AKAP12 was identified using a luciferase reporter assay. The results demonstrated that AGEs significantly suppressed cell proliferation and migration, while the expression of miR-146a decreased and the expression of AKAP12 increased. A luciferase reporter assay revealed that miR-146a could directly target AKAP12. Overexpression of miR-146a promoted cell proliferation and migration in an in vitro DFU model and also promoted the expression of HIF-1α, Wnt3a and β-catenin but suppressed the expression of AKAP12. Co-overexpression of miR-146a and AKAP12 reversed the effect of miR-146a on cell proliferation and migration. Our findings revealed that miR-146a directly targeted AKAP12 and promoted cell proliferation and migration in an in vitro DFU model. This study provides a new perspective for the study of miR-146a in the treatment of DFU.

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confidence: 99%

Overexpression of miR-146a promotes cell proliferation and migration in a model of diabetic foot ulcers by regulating the AKAP12 axis

2022

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Nerve action potential amplitude, a robust marker of diabetic peripheral neuropathy

Cited by 1 publication

References 10 publications

Overexpression of miR-146a promotes cell proliferation and migration in a model of diabetic foot ulcers by regulating the AKAP12 axis

Overexpression of miR-146a promotes cell proliferation and migration in a model of diabetic foot ulcers by regulating the AKAP12 axis

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