Abstract
ObjectivesOur previous study indicated that aerobic exercise relieves cognitive impairment in patients with vascular cognitive impairment (VCI) via regulating brain-derived neurotrophic factor (BDNF), but the mechanism is not yet clear. This study aimed to explore whether lncRNA taurine upregulated gene 1 (TUG1) participates in the process of VCI by regulating BDNF.MethodsThe expressions of TUG1 and BDNF in the serum of VCI patients were detected. The potential molecular mechanisms of TUG1 in regulating hippocampal neuronal apoptosis were explored in oxygen and glucose deprivation-induced (OGD-induced) hippocampal cell line HT22. The VCI mouse model was established, and TUG1 and BDNF were overexpressed via lentivirus injection. The cognitive impairment of mice was detected by the Morris water maze experiment after the aerobic exercise.ResultsThe level of TUG1 was elevated in the serum of VCI patients compared with the control group. The knockdown of TUG1 in OGD-induced HT22 cells increased BDNF level and decreased cell apoptosis, and the downregulation of BDNF restored the decreased cell apoptosis. RNA immunoprecipitation and RNA pull-down assays showed that TUG1 could bind to BDNF protein. The aerobic exercise alleviated cognitive impairment and inhibited hippocampal apoptosis in VCI mice. Meanwhile, the overexpression of TUG1 reversed the therapeutic effects of aerobic exercise on cognitive impairment.ConclusionsThe knockdown of TUG1 reduced hippocampal neuronal apoptosis and participates in the aerobic exercise-alleviated VCI, which was partly through regulating BDNF.
Highlights
Vascular cognitive impairment (VCI) is a cognitive impairment caused by vascular diseases, including mild cognitive impairment and dementia [1]
Aberrant expression of taurine upregulated gene 1 (TUG1) and brain-derived neurotrophic factor (BDNF) in the serum of VCI patients To investigate whether TUG1 and BDNF were differentially expressed during VCI, we detected the levels of TUG1 and BDNF in the serum of healthy people (n = 20) and VCI patients (n = 20)
The results of Quantitativereal-time PCR (qRT-PCR) showed that compared with healthy people, the level of TUG1 was observably elevated in the serum of VCI patients, which was 2.9 times higher than that in healthy people (Fig. 1a), while the mRNA level of BDNF was 0.52 times lower than that in healthy people (Fig. 1b)
Summary
Vascular cognitive impairment (VCI) is a cognitive impairment caused by vascular diseases, including mild cognitive impairment and dementia [1]. Studies have revealed that aerobic exercise improves cardiovascular function in adults and improves cognitive performance in patients with VCI [3,4,5]. Long non-coding RNAs (lncRNAs) are widely involved in various human pathological processes, including cerebrovascular diseases [6]. LncRNA taurine upregulated gene 1 (TUG1) is one of the earliest identified lncRNAs associated with human diseases, which plays a vital regulatory role in various diseases by regulating biological processes, such as cell proliferation, differentiation, and apoptosis [9,10,11]. Studies have shown that TUG1 may be related to the pathology of neurodegenerative diseases [12]. It is not explicit whether TUG1 is involved in the pathology of VCI
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