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 inGenes Vol. 10; no. 4; p. 313
Main Authors Wang, Tingting, Cheng, Yaling, Han, Haibin, Liu, Jie, Tian, Bo, Liu, Xiaocui
Format Journal Article
LanguageEnglish
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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.
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.)
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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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