MALAT1 and NEAT1 Are Neuroprotective During Hypoxic Preconditioning in the Mouse Hippocampus Possibly by Regulation of NR2B.

IF 1.6 4区 医学 Q4 BIOPHYSICS
Liping Wang, Gang Fu, Ruijuan Han, Peijia Fan, Jing Yang, Kerui Gong, Zhijun Zhao, Chunyang Zhang, Kai Sun, Guo Shao
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引用次数: 0

Abstract

Wang L, Fu G, Han R, Fan P, Yang J, Gong K, Zhao Z, Zhang C, Sun K, Shao GMALAT1 and NEAT1 Are Neuroprotective during Hypoxic Preconditioning in the Mouse Hippocampus Possibly by Regulation of NR2B High Alt Med Biol. 00:000-000, 2024. Background: The regulation of noncoding ribonucleic acid (ncRNA) has been shown to be involved in cellular and molecular responses to hypoxic preconditioning (HPC), a situation created by the induction of sublethal hypoxia in the brain. The ncRNAs metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) and nuclear paraspeckle assembly transcript 1 (NEAT1) are abundantly expressed in the brain, where they regulate the expression of various genes in nerve cells. However, the exact roles of MALAT1 and NEAT1 in HPC are not fully understood. Methods: A mouse model of acute repeated hypoxia was used as a model of HPC, and MALAT1 and NEAT1 levels in the hippocampus were measured using real-time polymerase chain reaction (PCR). The mRNA and protein levels of N-methyl-d-aspartate receptor subunit 2 B (NR2B) in the mouse hippocampus were measured using real-time PCR and western blotting, respectively. HT22 cells knocked-down for MALAT1 and NEAT1 were used for in vitro testing. Expression of NR2B, which is involved in nerve cell injury under ischemic and hypoxic conditions, was also evaluated. The levels of spectrin and cleaved caspase-3 in MALAT1 and NEAT1 knockdown HT22 cells under oxygen glucose deprivation/reperfusion (OGD/R) were determined by western blotting. Results: HPC increased the expression of MALAT1 and NEAT1 and decreased the expression of NR2B mRNA in the mouse hippocampus (p < 0.05). Knockdown of MALAT1 and NEAT1 increased both NR2B mRNA and protein levels nearly twofold and caused damage under OGD/R conditions in HT22 cells (p < 0.05). Conclusion: MALAT1 and NEAT1 exert neuroprotective effects by influencing the expression of NR2B.

MALAT1 和 NEAT1 可能通过调节 NR2B 在小鼠海马缺氧预处理过程中发挥神经保护作用
Wang L, Fu G, Han R, Fan P, Yang J, Gong K, Zhao Z, Zhang C, Sun K, Shao GMALAT1和NEAT1在小鼠海马缺氧预处理过程中具有神经保护作用,可能是通过调控NR2B实现的 High Alt Med Biol. 00:000-000, 2024.背景:非编码核糖核酸(ncRNA)的调控已被证明参与了细胞和分子对缺氧预处理(HPC)的反应。ncRNA 转移相关肺腺癌转录本 1(MALAT1)和核副颈组装转录本 1(NEAT1)在大脑中大量表达,它们调节神经细胞中各种基因的表达。然而,MALAT1 和 NEAT1 在 HPC 中的确切作用尚不完全清楚。研究方法使用实时聚合酶链反应(PCR)测定海马中 MALAT1 和 NEAT1 的水平。采用实时聚合酶链式反应(PCR)和蛋白印迹法分别测定了小鼠海马中 N-甲基-d-天冬氨酸受体亚基 2 B(NR2B)的 mRNA 和蛋白水平。体外测试使用了敲除 MALAT1 和 NEAT1 的 HT22 细胞。此外,还评估了参与缺血和缺氧条件下神经细胞损伤的 NR2B 的表达。在氧糖剥夺/再灌注(OGD/R)条件下,MALAT1 和 NEAT1 基因敲除 HT22 细胞中光谱蛋白和裂解的 Caspase-3 的水平通过 Western 印迹进行了测定。结果HPC增加了小鼠海马中MALAT1和NEAT1的表达,降低了NR2B mRNA的表达(p < 0.05)。敲除 MALAT1 和 NEAT1 会使 HT22 细胞中 NR2B mRNA 和蛋白水平增加近两倍,并在 OGD/R 条件下造成损伤(p < 0.05)。结论MALAT1和NEAT1通过影响NR2B的表达发挥神经保护作用。
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来源期刊
High altitude medicine & biology
High altitude medicine & biology 医学-公共卫生、环境卫生与职业卫生
CiteScore
3.80
自引率
9.50%
发文量
44
审稿时长
>12 weeks
期刊介绍: High Altitude Medicine & Biology is the only peer-reviewed journal covering the medical and biological issues that impact human life at high altitudes. The Journal delivers critical findings on the impact of high altitude on lung and heart disease, appetite and weight loss, pulmonary and cerebral edema, hypertension, dehydration, infertility, and other diseases. It covers the full spectrum of high altitude life sciences from pathology to human and animal ecology.
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