miR-194 Accelerates Apoptosis of Aβ1–42-Transduced Hippocampal Neurons by Inhibiting Nrn1 and Decreasing PI3K/Akt Signaling Pathway Activity
This article explores the mechanism of miR-194 on the proliferation and apoptosis of Aβ1–42-transduced hippocampal neurons. Aβ1–42-transduced hippocampal neuron model was established by inducing hippocampal neurons with Aβ1–42. MTT assay and flow cytometry were used to detect the viability and apopt...
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Published in | Genes Vol. 10; no. 4; p. 313 |
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Language | English |
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Abstract | This article explores the mechanism of miR-194 on the proliferation and apoptosis of Aβ1–42-transduced hippocampal neurons. Aβ1–42-transduced hippocampal neuron model was established by inducing hippocampal neurons with Aβ1–42. MTT assay and flow cytometry were used to detect the viability and apoptosis of hippocampal neurons, respectively. qRT-PCR was used to detect changes in miR-194 and Nrn1 expression after Aβ1–42 induction. Aβ1–42-transduced hippocampal neurons were transfected with miR-194 mimics and/or Nrn1 overexpression vectors. Their viability and neurite length were detected by MTT assay and immunofluorescence, respectively. Western blot was used to detect protein expression. Aβ1–42 inhibited Aβ1–42-transduced hippocampal neuron activity and promoted their apoptosis in a dose-dependent manner. miR-194 was upregulated and Nrn1 was downregulated in Aβ1–42-transduced hippocampal neurons (p < 0.05). Compared with the model group, Aβ1–42-transduced hippocampal neurons of the miR-194 mimic group had much lower activity, average longest neurite length, Nrn1, p-AkT, and Bcl-2 protein expression and had much higher Bax, Caspase-3, and Cleaved Caspase-3 protein expression. Compared with the model group, Aβ1–42-transduced hippocampal neurons of the LV-Nrn1 group had much higher activity, average longest neurite length, Nrn1, p-AkT, and Bcl-2 protein expression and had much lower Bax, Caspase-3, and Cleaved Caspase-3 protein expression. Nrn1 is a target gene of miR-194. miR-194 inhibited apoptosis of Aβ1–42-transduced hippocampal neurons by inhibiting Nrn1 and decreasing PI3K/AkT signaling pathway activity. |
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AbstractList | This article explores the mechanism of miR-194 on the proliferation and apoptosis of Aβ1–42-transduced hippocampal neurons. Aβ1–42-transduced hippocampal neuron model was established by inducing hippocampal neurons with Aβ1–42. MTT assay and flow cytometry were used to detect the viability and apoptosis of hippocampal neurons, respectively. qRT-PCR was used to detect changes in miR-194 and Nrn1 expression after Aβ1–42 induction. Aβ1–42-transduced hippocampal neurons were transfected with miR-194 mimics and/or Nrn1 overexpression vectors. Their viability and neurite length were detected by MTT assay and immunofluorescence, respectively. Western blot was used to detect protein expression. Aβ1–42 inhibited Aβ1–42-transduced hippocampal neuron activity and promoted their apoptosis in a dose-dependent manner. miR-194 was upregulated and Nrn1 was downregulated in Aβ1–42-transduced hippocampal neurons (p < 0.05). Compared with the model group, Aβ1–42-transduced hippocampal neurons of the miR-194 mimic group had much lower activity, average longest neurite length, Nrn1, p-AkT, and Bcl-2 protein expression and had much higher Bax, Caspase-3, and Cleaved Caspase-3 protein expression. Compared with the model group, Aβ1–42-transduced hippocampal neurons of the LV-Nrn1 group had much higher activity, average longest neurite length, Nrn1, p-AkT, and Bcl-2 protein expression and had much lower Bax, Caspase-3, and Cleaved Caspase-3 protein expression. Nrn1 is a target gene of miR-194. miR-194 inhibited apoptosis of Aβ1–42-transduced hippocampal neurons by inhibiting Nrn1 and decreasing PI3K/AkT signaling pathway activity. This article explores the mechanism of miR-194 on the proliferation and apoptosis of Aβ 1–42 -transduced hippocampal neurons. Aβ 1–42 -transduced hippocampal neuron model was established by inducing hippocampal neurons with Aβ 1–42 . MTT assay and flow cytometry were used to detect the viability and apoptosis of hippocampal neurons, respectively. qRT-PCR was used to detect changes in miR-194 and Nrn1 expression after Aβ 1–42 induction. Aβ 1–42 -transduced hippocampal neurons were transfected with miR-194 mimics and/or Nrn1 overexpression vectors. Their viability and neurite length were detected by MTT assay and immunofluorescence, respectively. Western blot was used to detect protein expression. Aβ 1–42 inhibited Aβ 1–42 -transduced hippocampal neuron activity and promoted their apoptosis in a dose-dependent manner. miR-194 was upregulated and Nrn1 was downregulated in Aβ 1–42 -transduced hippocampal neurons ( p < 0.05). Compared with the model group, Aβ 1–42 -transduced hippocampal neurons of the miR-194 mimic group had much lower activity, average longest neurite length, Nrn1, p-AkT, and Bcl-2 protein expression and had much higher Bax, Caspase-3, and Cleaved Caspase-3 protein expression. Compared with the model group, Aβ 1–42 -transduced hippocampal neurons of the LV-Nrn1 group had much higher activity, average longest neurite length, Nrn1, p-AkT, and Bcl-2 protein expression and had much lower Bax, Caspase-3, and Cleaved Caspase-3 protein expression. Nrn1 is a target gene of miR-194. miR-194 inhibited apoptosis of Aβ 1–42 -transduced hippocampal neurons by inhibiting Nrn1 and decreasing PI3K/AkT signaling pathway activity. |
Author | Wang, Tingting Cheng, Yaling Liu, Jie Tian, Bo Liu, Xiaocui Han, Haibin |
AuthorAffiliation | Psychiatric Department V, Qingdao Mental Health Center, No. 299, Nanjing Road, Shibei District, Qingdao 266000, China; wtt_920@163.com (T.W.); ling821118@sohu.com (Y.C.); hanhaibinqf@126.com (H.H.); jiejie19890128@126.com (J.L.); boyangqd@163.com (B.T.) |
AuthorAffiliation_xml | – name: Psychiatric Department V, Qingdao Mental Health Center, No. 299, Nanjing Road, Shibei District, Qingdao 266000, China; wtt_920@163.com (T.W.); ling821118@sohu.com (Y.C.); hanhaibinqf@126.com (H.H.); jiejie19890128@126.com (J.L.); boyangqd@163.com (B.T.) |
Author_xml | – sequence: 1 givenname: Tingting surname: Wang fullname: Wang, Tingting – sequence: 2 givenname: Yaling surname: Cheng fullname: Cheng, Yaling – sequence: 3 givenname: Haibin surname: Han fullname: Han, Haibin – sequence: 4 givenname: Jie surname: Liu fullname: Liu, Jie – sequence: 5 givenname: Bo surname: Tian fullname: Tian, Bo – sequence: 6 givenname: Xiaocui orcidid: 0000-0002-1791-4330 surname: Liu fullname: Liu, Xiaocui |
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Snippet | This article explores the mechanism of miR-194 on the proliferation and apoptosis of Aβ1–42-transduced hippocampal neurons. Aβ1–42-transduced hippocampal... This article explores the mechanism of miR-194 on the proliferation and apoptosis of Aβ 1–42 -transduced hippocampal neurons. Aβ 1–42 -transduced hippocampal... |
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SubjectTerms | 1-Phosphatidylinositol 3-kinase AKT protein Alzheimer's disease Apoptosis BAX protein Bcl-2 protein Binding sites Caspase-3 Cell cycle Flow cytometry Hippocampus Immunofluorescence MicroRNAs Neurons Pathogenesis Peptides Signal transduction |
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Title | miR-194 Accelerates Apoptosis of Aβ1–42-Transduced Hippocampal Neurons by Inhibiting Nrn1 and Decreasing PI3K/Akt Signaling Pathway Activity |
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