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施万细胞在白色脂肪组织中促成脱髓鞘性糖尿病性神经病变和神经末梢结构。

Schwann cells contribute to demyelinating diabetic neuropathy and nerve terminal structures in white adipose tissue.

作者信息

Willows Jake W, Gunsch Gilian, Paradie Emma, Blaszkiewicz Magdalena, Tonniges Jeffrey R, Pino Maria F, Smith Steven R, Sparks Lauren M, Townsend Kristy L

机构信息

Department of Neurological Surgery, The Ohio State University, Columbus, OH, USA.

Campus Microscopy and Imaging Facility, The Ohio State University, Columbus, OH, USA.

出版信息

iScience. 2023 Feb 13;26(3):106189. doi: 10.1016/j.isci.2023.106189. eCollection 2023 Mar 17.

DOI:10.1016/j.isci.2023.106189
PMID:36895649
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9989657/
Abstract

Peripheral neuropathy, which can include axonal degeneration and/or demyelination, impacts adipose tissues with obesity, diabetes, and aging. However, the presence of demyelinating neuropathy had not yet been explored in adipose. Both demyelinating neuropathies and axonopathies implicate Schwann cells (SCs), a glial support cell that myelinates axons and contributes to nerve regeneration after injury. We performed a comprehensive assessment of SCs and myelination patterns of subcutaneous white adipose tissue (scWAT) nerves, and changes across altered energy balance states. We found that mouse scWAT contains both myelinated and unmyelinated nerves and is populated by SCs, including SCs that were associated with synaptic vesicle-containing nerve terminals. BTBR mice, a model of diabetic peripheral neuropathy, exhibited small fiber demyelinating neuropathy and alterations in SC marker gene expression in adipose that were similar to obese human adipose. These data indicate that adipose SCs regulate the plasticity of tissue nerves and become dysregulated in diabetes.

摘要

周围神经病变,可包括轴突变性和/或脱髓鞘,会影响肥胖、糖尿病和衰老状态下的脂肪组织。然而,脂肪组织中脱髓鞘性神经病变的存在尚未得到研究。脱髓鞘性神经病变和轴索性神经病变都与施万细胞(SCs)有关,施万细胞是一种神经胶质支持细胞,它能使轴突形成髓鞘,并在损伤后促进神经再生。我们对皮下白色脂肪组织(scWAT)神经的施万细胞和髓鞘形成模式,以及能量平衡状态改变时的变化进行了全面评估。我们发现,小鼠scWAT包含有髓神经和无髓神经,且有施万细胞分布,包括与含有突触小泡的神经末梢相关的施万细胞。BTBR小鼠是糖尿病性周围神经病变的模型,表现出小纤维脱髓鞘性神经病变,且脂肪组织中施万细胞标记基因表达发生改变,这与肥胖人类脂肪组织中的情况相似。这些数据表明,脂肪组织中的施万细胞调节组织神经的可塑性,且在糖尿病中会失调。

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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d97e/9989657/5a7393a5c4d1/fx1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d97e/9989657/aa6bf7770594/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d97e/9989657/b289c01d0c79/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d97e/9989657/e3d504a302a3/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d97e/9989657/285f02ca41b0/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d97e/9989657/cd822a9d0372/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d97e/9989657/2da8a94d66d0/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d97e/9989657/1713a8f80613/gr7.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d97e/9989657/c2b92b37b3f3/gr9.jpg

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