Effects of Fdft 1 gene silencing and VD3 intervention on lung injury in hypoxia-stressed rats

Pu, Xiongming; Lin, Xue; Qi, Yinglian; Li, Yinglian; Li, Tiantian; Liu, Yang; Wei, Deng-Bang

doi:10.1007/s13258-022-01284-3

Genes Genom

2022

DOI: 10.1007/s13258-022-01284-3

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Effects of Fdft 1 gene silencing and VD3 intervention on lung injury in hypoxia-stressed rats

Xiongming Pu

Xue Lin

Yinglian Qi

et al.

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2023

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Cited by 1 publication

References 38 publications

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S1PR2 Regulates Autophagy Through the AKT/mTOR Pathway to Promote Pathological Damage in Alzheimer’s Disease

Wang,

Huang,

Huang

et al. 2023

JAD

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Background: Alzheimer’s disease (AD) is a fatal and debilitating neurodegenerative disease. Sphingosine-1-phosphate receptor 2 (S1PR2), one of the receptors of S1P, is a key regulatory factor for various diseases. Objective: This study aimed to explore the role and possible mechanism of S1PR2 in AD. Methods: S1PR2 expression in the AD mice was detected, and after intervening S1PR2 expression with sh-S1PR2 in AD mice, the behavioral changes, pathological lesions of the hippocampus, autophagy level, and AKT/mTOR pathway activation were analyzed. Furthermore, SH-SY5Y cells were induced by Aβ25-35 to construct an AD cell model, and the effects of sh-S1PR2 on proliferation, apoptosis, autophagy, and AKT/mTOR pathway of AD cells were investigated. In addition, the effects of pathway inhibitor rapamycin on model cells were further analyzed. Results: The expression of S1PR2 was significantly increased in AD mice, the sh-S1PR2 significantly improved behavioral dysfunction, alleviated pathological injury of the hippocampus, increased the number of neurons, and inhibited Aβ production and p-tau expression, showing a positive effect on the AD pathology. In addition, silencing of S1PR2 expression significantly promoted the autophagy level and inhibited the activation of the AKT/mTOR pathway in AD model mice. In vitro experiments further confirmed that sh-S1PR2 promoted cell proliferation, inhibited apoptosis, relieved cytopathology, promoted autophagy, and inhibited the activation of the AKT/mTOR pathway in the cell model. The use of rapamycin further confirmed the role of AKT/mTOR pathway-mediated autophagy in the regulation of AD by S1PR2. Conclusion: S1PR2 promoted AD pathogenesis by inhibiting autophagy through the activation of AKT/mTOR pathway.

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S1PR2 Regulates Autophagy Through the AKT/mTOR Pathway to Promote Pathological Damage in Alzheimer’s Disease

Wang,

Huang,

Huang

et al. 2023

JAD

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Effects of Fdft 1 gene silencing and VD3 intervention on lung injury in hypoxia-stressed rats

Cited by 1 publication

References 38 publications

S1PR2 Regulates Autophagy Through the AKT/mTOR Pathway to Promote Pathological Damage in Alzheimer’s Disease

S1PR2 Regulates Autophagy Through the AKT/mTOR Pathway to Promote Pathological Damage in Alzheimer’s Disease

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