miR-125a-5p in astrocytes attenuates peripheral neuropathy in type 2 diabetic mice through targeting TRAF6

Kasimu, Aziguli; Apizi, Xierenguli; Talifujiang, Dilibaier; Ma, Xin; Fang, Liping; Zhou, Xiangling

doi:10.1016/j.endinu.2021.01.007

Cited by 7 publications

(1 citation statement)

References 29 publications

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“…Forced introduction of miR-125a-5p into astrocytes reduces TRAF6, p-JNK1, and p-JNK2 and suppresses astrocyte activation, rendering miR-125a-5p a possible pharmacological target [25,26]. Elevated TRAF6 levels stimulate neuroinflammation owing to increased TRAF6 binding to K63, as neuropathic pain reduces TRAF6 protein levels in the spinal cord by activating and impairing autophagy [24].…”

Section: Discussionmentioning

confidence: 99%

Effects of Pain Relief Through Minimal Exercise Intervention in a Rat Model of Neuropathic Pain

Sumizono,

Yoshizato,

Imai

et al. 2024

Cureus

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We aimed to minimize the frequency of exercise intervention and test the efficacy of pain relief. We also investigated the mechanism of neuropathic pain to determine the best frequency of pain relief for neuropathic pain. The chronic constriction injury (CCI) rat model was randomly divided into three groups: exercise (Ex), No-Ex, and normal. The treadmill exercise intervention was administered, and the 50% withdrawal threshold was assessed using the Von Frey Test. Ionized calcium-binding adaptor molecule 1 (IBA1), glial fibrillary acidic protein (GFAP), brain-derived neurotrophic factor (BDNF), C-C chemokine receptor type 2 (CCR2), and tumor necrosis factor receptor-associated factor 6 (TRAF6) activation was determined through immunohistochemistry. In the brain, we examined the increased expression of β-endorphin/met-enkephalin in the gray matter of the midbrain aqueduct. Co-expression of CCR2, IBA1, and Neu-N was observed in the spinal cord dorsal horn by immunofluorescence staining. The 50% pain response threshold was significantly lower in the Ex group than in the No-Ex group at five weeks post-CCI, indicating a high analgesic effect. In the dorsal horn of the spinal cord, IBA1 and GFAP were significantly decreased in the Ex group than in the No-Ex group at five weeks post-CCI. However, no significant difference in activation of BDNF, CCR2, and TRAF6 was observed. In the midbrain, the Ex group showed a significant increase compared to the No-Ex group. In summary, our results suggest that in minimal-exercise intervention, neuropathic pain relief is achieved by activation of the descending pain inhibitory system in the midbrain.

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Section: Discussionmentioning

confidence: 99%

Effects of Pain Relief Through Minimal Exercise Intervention in a Rat Model of Neuropathic Pain

Sumizono,

Yoshizato,

Imai

et al. 2024

Cureus

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Glial cell alterations in diabetes-induced neurodegeneration

Llorián-Salvador,

Cabeza-Fernández,

Gomez-Sanchez

et al. 2024

Cell. Mol. Life Sci.

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Type 2 diabetes mellitus is a global epidemic that due to its increasing prevalence worldwide will likely become the most common debilitating health condition. Even if diabetes is primarily a metabolic disorder, it is now well established that key aspects of the pathogenesis of diabetes are associated with nervous system alterations, including deleterious chronic inflammation of neural tissues, referred here as neuroinflammation, along with different detrimental glial cell responses to stress conditions and neurodegenerative features. Moreover, diabetes resembles accelerated aging, further increasing the risk of developing age-linked neurodegenerative disorders. As such, the most common and disabling diabetic comorbidities, namely diabetic retinopathy, peripheral neuropathy, and cognitive decline, are intimately associated with neurodegeneration. As described in aging and other neurological disorders, glial cell alterations such as microglial, astrocyte, and Müller cell increased reactivity and dysfunctionality, myelin loss and Schwann cell alterations have been broadly described in diabetes in both human and animal models, where they are key contributors to chronic noxious inflammation of neural tissues within the PNS and CNS. In this review, we aim to describe in-depth the common and unique aspects underlying glial cell changes observed across the three main diabetic complications, with the goal of uncovering shared glial cells alterations and common pathological mechanisms that will enable the discovery of potential targets to limit neuroinflammation and prevent neurodegeneration in all three diabetic complications. Diabetes and its complications are already a public health concern due to its rapidly increasing incidence, and thus its health and economic impact. Hence, understanding the key role that glial cells play in the pathogenesis underlying peripheral neuropathy, retinopathy, and cognitive decline in diabetes will provide us with novel therapeutic approaches to tackle diabetic-associated neurodegeneration. Graphical abstract

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Depleted miR-125a-5p Causes Vascular Endothelial Cell Dysfunction in Deep Vein Thrombosis by Targeting Angiopoietin 2

Huang

Zhang³

et al. 2022

Indian J Hematol Blood Transfus

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miR-125a-5p in astrocytes attenuates peripheral neuropathy in type 2 diabetic mice through targeting TRAF6

Cited by 7 publications

References 29 publications

Effects of Pain Relief Through Minimal Exercise Intervention in a Rat Model of Neuropathic Pain

Effects of Pain Relief Through Minimal Exercise Intervention in a Rat Model of Neuropathic Pain

Glial cell alterations in diabetes-induced neurodegeneration

Depleted miR-125a-5p Causes Vascular Endothelial Cell Dysfunction in Deep Vein Thrombosis by Targeting Angiopoietin 2

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