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Overexpression of miR-221 stimulates proliferation of rat neural stem cell with activating Phosphatase and tensin homolog/protein kinase B signaling pathway.
Chen, Yanze; Gao, Yunan; Lian, Ying; Li, Chengkun; Qu, Chen; Jiang, Xiaowen.
Afiliação
  • Chen Y; Department of Stomatology, the First People's Hospital of Chenzhou, Southern Medical University and Institute of Translation Medicine, University of China South, Chenzhou, Hunan.
  • Gao Y; Department of Orthodontics, Stomatological Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi.
  • Lian Y; Departments of Electrocardiogram Room.
  • Li C; Internal neurology, the First People's Hospital of Chenzhou, Chenzhou, Hunan.
  • Qu C; Department of Stomatology, Affiliated Children's Hospital, Chongqing Medical University, Chongqing.
  • Jiang X; Department of Stomatology, the First People's Hospital of Chenzhou, Southern Medical University and Institute of Translation Medicine, University of China South, Chenzhou, Hunan.
Neuroreport ; 31(14): 1015-1023, 2020 10 07.
Article em En | MEDLINE | ID: mdl-32858649
ABSTRACT
Neural stem cells (NSCs) are self-renewing, multipotent cells, and remain in our brains throughout life. They could be activated by brain damage and involved in the central nervous system (CNS) repair and motor functional recovery. Previous research demonstrated that miR-221 could regulate proliferation, differentiation, and survival. However, the effect of miR-221 on NSCs remains unknown. In this study, we showed that overexpression of miR-221 inhibited the expression of phosphatase and tensin homolog (PTEN) protein and increased the phosphorylation level of protein kinase B (AKT). More importantly, an AKT-specific inhibitor abolished the effect of miR-221 on the phosphorylation level of AKT. 5-Bromo-2-deoxyUridine (BrdU) incorporation assay and Cyclin D1 expression showed that miR-221 overexpression further promoted the NSCs proliferation. However, knocking down miR-221 inhibited cell proliferation. The AKT-specific inhibitor also blocked the proliferative efficiency of miR-221. These results demonstrated that miR-221 overexpression promoted the proliferation of cultured rat NSCs, for which the PTEN/AKT pathway activation was one possible mechanism. Our research may provide a novel investigating strategy to improve stem cell treatment for CNS diseases.
Assuntos

Texto completo: 1 Base de dados: MEDLINE Assunto principal: MicroRNAs / Proliferação de Células / PTEN Fosfo-Hidrolase / Proteínas Proto-Oncogênicas c-akt / Células-Tronco Neurais Limite: Animals Idioma: En Revista: Neuroreport Assunto da revista: NEUROLOGIA Ano de publicação: 2020 Tipo de documento: Article

Texto completo: 1 Base de dados: MEDLINE Assunto principal: MicroRNAs / Proliferação de Células / PTEN Fosfo-Hidrolase / Proteínas Proto-Oncogênicas c-akt / Células-Tronco Neurais Limite: Animals Idioma: En Revista: Neuroreport Assunto da revista: NEUROLOGIA Ano de publicação: 2020 Tipo de documento: Article