2. Academic Validation
  3. Up-regulation of lncRNA WT1-AS ameliorates Aβ-stimulated neuronal injury through modulation of miR-186-5p/CCND2 axis in Alzheimer's disease

Up-regulation of lncRNA WT1-AS ameliorates Aβ-stimulated neuronal injury through modulation of miR-186-5p/CCND2 axis in Alzheimer's disease

  • Cell Mol Biol (Noisy-le-grand). 2024 Jan 31;70(1):200-206. doi: 10.14715/cmb/2024.70.1.27.
Yun Tang 1,  Xiaojiu Zhang 2,  Shihui Wang 3,  Lu Liu 4,  Qing Wang 5,  Yufeng Liu 6,  Yadong Yu 7,  Qijin Zhai 8
Affiliations

Affiliations

  • 1 Department of Neurology, The Affiliated Huai'an Hospital of Xuzhou Medical University, Huai'an 223002, Jiangsu, China. iyun-tang@outlook.com.
  • 2 Department of Neurology, The Affiliated Huai'an Hospital of Xuzhou Medical University, Huai'an 223002, Jiangsu, China. zxj7418695@163.com.
  • 3 Department of Neurology, Siyang Hospital of Traditional Chinese Medicine, Siyang 223700, Jiangsu, China. 190819904@qq.com.
  • 4 Department of Neurology, The Affiliated Huai'an Hospital of Xuzhou Medical University, Huai'an 223002, Jiangsu, China. ll18796201519@163.com.
  • 5 Department of Neurology, The Affiliated Huai'an Hospital of Xuzhou Medical University, Huai'an 223002, Jiangsu, China. 291667754@qq.com.
  • 6 Department of Neurology, The Affiliated Huai'an Hospital of Xuzhou Medical University, Huai'an 223002, Jiangsu, China. lyf996226@163.com.
  • 7 Department of Emergency, Lianshui People's Hospital Affiliated to Kangda College of Nanjing Medical University, Lianshui 223400, Jiangsu, China. Ls_yyd@163.com.
  • 8 Department of Neurology, The Affiliated Huai'an Hospital of Xuzhou Medical University, Huai'an 223002, Jiangsu, China. qjzhai1983@163.com.
PMID: 38372094 DOI: 10.14715/cmb/2024.70.1.27
Abstract

As a common neurodegenerative disorder, Alzheimer's disease (AD) seriously threatens human life. Long non-coding RNAs (lncRNAs) exhibit essential functions in AD development. Nevertheless, the detailed effects and possible mechanisms of lncRNA Wilms tumor 1 Antisense RNA (WT1-AS) in AD are largely unknown. In our studies, a total of 30 serum samples from AD patients were collected, and WT1-AS expressions were detected through qRT-PCR analysis. Additionally, an in vitro AD model was constructed by treating Aβ1-42 in human neuroblastoma cells. Functional assays were implemented to assess the impacts of WT1-AS on Aβ1-42-stimulated human neuroblastoma cell proliferation together with Apoptosis. Moreover, relationship of WT1-AS, MicroRNA (miR)-186-5p as well as cyclin D2 (CCND2) could be predicted through bioinformatics tools as well as proved via dual-luciferase reporter experiments. Our results showed that WT1-AS together with CCND2 were low-expressed, while miR-186-5p presented high expression in AD serum samples together with Aβ1-42-stimulated human neuroblastoma cells. WT1-AS over-expression or miR-186-5p depletion notably promoted the proliferation, reduced the Apoptosis, and decreased the p-Tau protein expressions of human neuroblastoma cells induced with Aβ1-42. Moreover, miR-186-5p combined with WT1-AS, and CCND2 was modulated by miR-186-5p. Furthermore, CCND2 elevation partially offsets the impacts of miR-186-5p elevation on Aβ1-42-stimulated cell proliferation as well as Apoptosis mediated with WT1-AS up-regulation. Our results indicated that up-regulation of lncRNA WT1-AS ameliorated Aβ-stimulated neuronal damage through modulating miR-186-5p/CCND2 axis, offering a novel direction for AD therapy.

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