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.
Highlights
Alzheimer’s disease (AD) is an age-related neurodegenerative disease with clinical features such as progressive cognitive impairment and psychomotor disorders [1,2]
These results indicated that the expression of miR-194 directly the proliferation and apoptosis of
This study first studied the effects of miR-194 on the biological behavior of Aβ1–42 -transduced hippocampal neurons, and the results suggested that miR-194 suppressed Aβ1–42 -transduced hippocampal neuron activity and accelerated their apoptosis by targeting the inhibition of Nrn1 expression
Summary
Alzheimer’s disease (AD) is an age-related neurodegenerative disease with clinical features such as progressive cognitive impairment and psychomotor disorders [1,2]. The pathogenesis of Alzheimer’s disease involves a variety of factors, including genetic factors, vascular disease, and malnutrition [3,4,5]. AD is mainly characterized by the formation of insoluble senile plaques [7]. Β-amyloid (Aβ), a cleavage product of the amyloid precursor protein (APP), is the main component of insoluble senile plaques, whose deposition is neurotoxic and could induce apoptosis of neurons [8,9,10]. The prevention and treatment of AD are still a major clinical problem all over the world. The discovery of exact molecular pathogenesis has important clinical implications for AD patients
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