Suppr超能文献

诱导多能干细胞分化的异常神经祖细胞部分模拟了 TSC2 神经发育异常。

Abnormal Neural Progenitor Cells Differentiated from Induced Pluripotent Stem Cells Partially Mimicked Development of TSC2 Neurological Abnormalities.

机构信息

Department of Neurology, First Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong 510080, P.R. China; Department of Neurology, Seventh Affiliated Hospital of Sun Yat-sen University, Shenzhen, Guangdong 518017, P.R. China.

Department of Neurology, First Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong 510080, P.R. China; Department of Neurology, The Central Hospital of Wuhan, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430014, P.R. China.

出版信息

Stem Cell Reports. 2017 Apr 11;8(4):883-893. doi: 10.1016/j.stemcr.2017.02.020. Epub 2017 Mar 23.

Abstract

Tuberous sclerosis complex (TSC) is a disease featuring devastating and therapeutically challenging neurological abnormalities. However, there is a lack of specific neural progenitor cell models for TSC. Here, the pathology of TSC was studied using primitive neural stem cells (pNSCs) from a patient presenting a c.1444-2A>C mutation in TSC2. We found that TSC2 pNSCs had higher proliferative activity and increased PAX6 expression compared with those of control pNSCs. Neurons differentiated from TSC2 pNSCs showed enlargement of the soma, perturbed neurite outgrowth, and abnormal connections among cells. TSC2 astrocytes had increased saturation density and higher proliferative activity. Moreover, the activity of the mTOR pathway was enhanced in pNSCs and induced in neurons and astrocytes. Thus, our results suggested that TSC2 heterozygosity caused neurological malformations in pNSCs, indicating that its heterozygosity might be sufficient for the development of neurological abnormalities in patients.

摘要

结节性硬化症(TSC)是一种具有破坏性且治疗极具挑战性的神经异常疾病。然而,目前缺乏用于 TSC 的特定神经祖细胞模型。本研究使用携带 TSC2 c.1444-2A>C 突变的患者来源的原始神经干细胞(pNSCs)来研究 TSC 的病理学。我们发现与对照 pNSCs 相比,TSC2 pNSCs 具有更高的增殖活性和增加的 PAX6 表达。源自 TSC2 pNSCs 的神经元表现出胞体增大、突起生长紊乱以及细胞间异常连接。TSC2 星形胶质细胞的饱和密度增加,增殖活性增强。此外,mTOR 通路的活性在 pNSCs 中增强,并在神经元和星形胶质细胞中诱导。因此,我们的结果表明 TSC2 杂合性导致 pNSCs 中的神经畸形,表明其杂合性可能足以导致患者的神经发育异常。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fdda/5390135/1db6f609707c/gr1.jpg

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验