دورية أكاديمية

Role and mechanism of miRNA-29a/PTEN pathway in neuronal network damage caused by aluminum

التفاصيل البيبلوغرافية
العنوان: Role and mechanism of miRNA-29a/PTEN pathway in neuronal network damage caused by aluminum
المؤلفون: Changxin XIANG, Yingchao HAN, Meng LI, Liyuan LU, Qiao NIU, Huifang ZHANG
المصدر: 环境与职业医学, Vol 39, Iss 4, Pp 397-403 (2022)
بيانات النشر: Editorial Committee of Journal of Environmental and Occupational Medicine, 2022.
سنة النشر: 2022
المجموعة: LCC:Medicine (General)
LCC:Toxicology. Poisons
مصطلحات موضوعية: aluminum, microrna-29a, phosphatase and tensin homolog deleted on chromosome ten, neuron network damage, Medicine (General), R5-920, Toxicology. Poisons, RA1190-1270
الوصف: BackgroundAluminum can cause synaptic plasticity damage in the hippocampus, probably due to blocked interneuronal signal transmission. MicroRNA-29a (miR-29a) can target phosphatase and tensin homolog deleted on chromosome ten (PTEN) expression and participate in the generation of neuronal networks, and may be involved in the effect of aluminum on the electrical activity of neuronal networks.ObjectiveTo study the role and mechanism of miR-29a-targeted PTEN in aluminum-induced neuronal network injury in primary hippocampal neurons of ICR mice treated with maltol aluminum [Al(mal)3] in vitro.MethodsPrimary hippocampal neurons of ICR mice born within 24 h were cultured in vitro. The purity of neurons was determined by labeling neuron-specific microtubule-associated protein 2 (MAP2) by immunofluorescence staining on day six of the culture; neurons were treated with different concentrations of Al(mal)3, and divided into a control group, and 10, 20, and 40 μmol·L−1 Al(mal)3 groups, and neuronal cell viability was detected by CCK-8 method. Al(mal)3 at 20 μmol·L−1 was selected for subsequent experiments to establish a neuronal network injury model for intervention. The lentivirus infection method was used to transfect miR-29a into neurons, which were divided into mNG, mNG+20 μmol·L−1 Al(mal)3, miR-29a, and miR-29a+20 μmol·L−1 Al(mal)3 groups, and micro-electrode array (MEA) was used to analyze the firing of neuronal network. The expressions of miR-29a and PTEN mRNA in each group were detected by real-time PCR (RT-PCR), and the expression of PTEN protein in each group was detected by Western blotting.ResultsThe purity of primary mouse hippocampal neurons was greater than 90%, and the viability of the neurons was above 80% in all groups. At 48 h of the designed Al(mal)3 treatments, the changes in spike frequency, burst frequency, network burst frequency, and synchrony index of neurons cultivated on MEA plates in the control group were 207.56%±38.70%, 73.19%±46.43%, 75.42%±33.04%, and 117.13%±15.54%, respectively; the Al(mal)3 groups’ neuronal network electrical activity showed a decreasing trend. Compared with the control group, the spike frequency, burst frequency, network burst frequency, and synchrony index of the 20 and 40 μmol·L−1 Al(mal)3 groups significantly decreased (The changes were 171.70%±28.08%, 49.20%±23.23%, 50.20%±18.18%, and 85.45%±20.30%; 150.68%±26.15%, 43.43%±15.54%, 52.05%±26.31%, and 26.80%±8.29%, respectively, P < 0.05). Compared with the control group (1.00), the miR-29a relative expression levels were significantly decreased in the 20 μmol·L−1 Al(mal)3 group (0.74±0.09) and the 40 μmol·L−1 Al(mal)3 group (0.62±0.12) (P < 0.05); the relative expression levels of PTEN mRNA were significantly increased in the 20 μmol·L−1 Al(mal)3 group (1.32±0.12) and the 40 μmol·L−1 Al(mal)3 group (1.48±0.11) (P < 0.05); the PTEN protein relative expression levels (1.29±0.12 and 1.82±0.10, respectively) were also significantly increased (P < 0.05). By overexpressing miR-29a in mouse primary hippocampal neurons, the spike frequency, burst frequency, and network burst frequency were significantly higher in the miR-29a group compared with the mNG group (The changes were 252.80%±62.03%, 171.65%±56.30%, and 197.75%±27.12%, respectively, P
نوع الوثيقة: article
وصف الملف: electronic resource
اللغة: English
Chinese
تدمد: 2095-9982
العلاقة: http://www.jeom.org/article/cn/10.11836/JEOM21327Test; https://doaj.org/toc/2095-9982Test
DOI: 10.11836/JEOM21327
الوصول الحر: https://doaj.org/article/3455098af6ee4d358a3816b8cbdd8016Test
رقم الانضمام: edsdoj.3455098af6ee4d358a3816b8cbdd8016
قاعدة البيانات: Directory of Open Access Journals
الوصف
تدمد:20959982
DOI:10.11836/JEOM21327