Apelin receptor homodimer inhibits apoptosis in vascular dementia

Wang, Dexiu; Wang, Yuliang; Shan, Meiyan; Chen, Jing; Wang, Huannan; Sun, Baoqi; Jin, Chengwen; Li, Xin; Yin, Yue; Song, Chao; Xiao, Changhao; Li, Jianshe; Wang, Taiqian; Cai, Xin

doi:10.1016/j.yexcr.2021.112739

Cited by 10 publications

(10 citation statements)

References 39 publications

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“… 26 Multiple studies used the OGD/R in vitro model in neurons for the investigation of vascular dementia. 26 27 28 In our study, miR-322-5p showed a significantly low expression in OGD/R-treated NRNs. We then upregulated the expression of miR-322-5p and found that OGD/R-induced cell injury was alleviated by miR-322-5p overexpression.…”

Section: Discussionsupporting

confidence: 51%

MiR-322-5p Alleviates Cell Injury and Impairment of Cognitive Function in Vascular Dementia by Targeting TSPAN5

et al. 2022

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Purpose As the population ages, the incidence of clinical dementia has been rising around the world. It has been reported that microRNAs act as key diagnostic biomarkers and targets for various neurological conditions, including dementia. MiR-322-5p has been revealed to play an important role in multiple diseases. In this study, we aimed to investigate the role and regulatory mechanism of miR-322-5p in vascular dementia. Materials and Methods In this study, neonatal rat neurons (NRNs) were subjected to oxygen-glucose deprivation/reoxygenation (OGD/R) to induce cell injury. The animals were subjected to permanent bilateral occlusion of the carotid arteries (2-vessel occlusion, 2VO) to induce the model of chronic brain hypoperfusion. Results MiR-322-5p expression was significantly downregulated in the neurons exposed to OGD/R and the hippocampi of 2VO rats. Overexpression of miR-322-5p ameliorated cell apoptosis and the inflammatory response in vitro. In a mechanistic study, miR-322-5p was confirmed to directly target and negatively regulate tetraspanin 5 (TSPAN5) in cultured NRNs. Moreover, overexpression of TSPAN5 could counteract the effects of miR-322-5p overexpression on cell apoptosis and the inflammatory response in OGD/R-treated neurons. More importantly, miR-322-5p improved cognitive ability and inhibited inflammatory production in 2VO rats. Conclusion Overall, the results suggest that miR-322-5p alleviates vascular dementia development by targeting TSPAN5. This discovery may provide a potential therapeutic target for dementia.

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Section: Discussionsupporting

confidence: 51%

MiR-322-5p Alleviates Cell Injury and Impairment of Cognitive Function in Vascular Dementia by Targeting TSPAN5

et al. 2022

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“…Cell death is a much studied final common path in human neuronal in vitro models of cerebral ischemia. A total of 59 studies in undifferentiated (Agudo-Lopez et al 2010 ; Castri et al 2014 ; Chen et al 2019 ; Dong et al 2019 , 2021 ; Du et al 2012 ; Feng et al 2021 ; Gao et al 2017 , 2020 ; He et al 2014 ; Hu et al 2020 ; Huang et al 2018 , 2021 ; Jia et al 2021 ; Lee et al 2013 ; Li and Ma 2020 ; Li et al 2020a ; Liu et al 2019b ; Lu et al 2019 ; Luan et al 2013 ; Marutani et al 2012 ; Meng et al 2021 ; Nampoothiri and Rajanikant 2019 ; Niu et al 2018 ; Park et al 2017 ; Ruan et al 2020 ; Shan et al 2022 ; Shi et al 2021 ; Song et al 2019 ; Tian et al 2020 ; Wang et al 2013 , 2017 , 2018b , c , 2019b , c , 2020b , 2021a , b ; Wang and Xu 2021 ; Wen et al 2020 ; Wu et al 2020a , b ; Xing et al 2021 ; Xu et al 2020a , b ; Yan et al 2015 , 2020 ; Yang et al 2014 , 2021a ; Yao et al 2019 ; Yi et al 2020 ; Zappala et al 2021 ; Zhang et al 2016a , b ,…”

Section: Resultsmentioning

confidence: 99%

“…Apoptosis can be triggered through an intrinsic pathway which is regulated by B-cell lymphoma 2 (BCL-2) protein family and is activated by internal signals. The expression of anti-apoptotic BCL-2 has been investigated in 25 studies using undifferentiated SH-SY5Y cells (Chang et al 2017 ; Dong et al 2019 ; Feng et al 2021 ; Gao et al 2020 ; Guo 2019 ; He et al 2014 ; Hu et al 2020 ; Huang et al 2018 ; Li et al 2019b , 2020a ; Liu et al 2018 , 2020 ; Wang et al 2013 , 2019c , 2020b , 2021a , b ; Wu et al 2020a ; Xu et al 2020b ; Yan et al 2020 ; Zhang et al 2016b ; Zhao and Wang 2020 ; Zhi et al 2020 ; Zhou et al 2019 ) and in one study using differentiated SH-SY5Y cells (Sriwastva et al 2020 ). It was found that BCL-2 decreased during and after ischemia/hypoxia.…”

Section: Resultsmentioning

confidence: 99%

“…The caspase family is extensively investigated in relation to apoptosis in ischemia/hypoxia. In studies with undifferentiated SH-SY5Y cells (n = 39), two members of the caspase family (caspase-3 and caspase-9) were increased during and after ischemia/hypoxia (Castri et al 2014 ; Chang et al 2017 ; Chen et al 2015 , 2019 ; Dong et al 2019 ; Du et al 2012 ; Feng et al 2021 ; Gao et al 2020 ; Hong et al 2017 ; Huang et al 2018 ; Jia et al 2021 ; Li and Ma 2020 ; Lin et al 2020 ; Liu et al 2018 ; Marutani et al 2012 ; Park et al 2017 ; Ruan et al 2020 ; Shan et al 2022 ; Shi et al 2020 ; Song et al 2019 ; Tan et al 2021 ; Wang et al 2018a , c , 2019b , 2021a , b ; Wen et al 2020 ; Wu et al 2020a ; Xing et al 2021 ; Xu et al 2020b ; Yan et al 2020 ; Yi et al 2020 ; Yin et al 2021 ; Zappala et al 2021 ; Zhang et al 2016a , b ; Zhao and Wang 2020 ; Zhi et al 2020 ; Zuo et al 2020 ). Increased expression of caspase-3, -6, -7 after ischemia/hypoxia was found in differentiated SH-SY5Y (n = 5) (Cheng et al 2014 ; Sriwastva et al 2020 ; Xu et al 2020a ; Zhang et al 2019b ; Zhou et al 2014 ).…”

Section: Resultsmentioning

confidence: 99%

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Neuronal Responses to Ischemia: Scoping Review of Insights from Human-Derived In Vitro Models

2023

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Translation of neuroprotective treatment effects from experimental animal models to patients with cerebral ischemia has been challenging. Since pathophysiological processes may vary across species, an experimental model to clarify human-specific neuronal pathomechanisms may help. We conducted a scoping review of the literature on human neuronal in vitro models that have been used to study neuronal responses to ischemia or hypoxia, the parts of the pathophysiological cascade that have been investigated in those models, and evidence on effects of interventions. We included 147 studies on four different human neuronal models. The majority of the studies (132/147) was conducted in SH-SY5Y cells, which is a cancerous cell line derived from a single neuroblastoma patient. Of these, 119/132 used undifferentiated SH-SY5Y cells, that lack many neuronal characteristics. Two studies used healthy human induced pluripotent stem cell derived neuronal networks. Most studies used microscopic measures and established hypoxia induced cell death, oxidative stress, or inflammation. Only one study investigated the effect of hypoxia on neuronal network functionality using micro-electrode arrays. Treatment targets included oxidative stress, inflammation, cell death, and neuronal network stimulation. We discuss (dis)advantages of the various model systems and propose future perspectives for research into human neuronal responses to ischemia or hypoxia. Graphical Abstract

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“…In studies by Wang et al, APJ heterodimer decreased the level of cleaved caspase-9 and caspase-3 through the guanine nucleotide-binding protein Gαi1 and Gαq3 signalling pathway, at the same time as increasing the number of neurons in the SH-SY5Y cell line. Additionally, the anti-apoptotic effect of apelin-13 in rat vascular dementia models was demonstrated [70]. The results presented by Xu et al showed that apelin-13 attenuates brain injury following subarachnoid haemorrhage (SAH) in rats.…”

Section: Nervous Systemmentioning

confidence: 97%

The Apelinergic System: Apelin, ELABELA, and APJ Action on Cell Apoptosis: Anti-Apoptotic or Pro-Apoptotic Effect?

Respekta

Pich

Dawid

et al. 2022

Cells

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The apelinergic system comprises two peptide ligands, apelin and ELABELA, and their cognate G-protein-coupled receptor, the apelin receptor APJ. Apelin is a peptide that was isolated from bovine stomach extracts; the distribution of the four main active forms, apelin-36, -17, -13, and pyr-apelin-13 differs between tissues. The mature form of ELABELA-32 can be transformed into forms called ELABELA-11 or -21. The biological function of the apelinergic system is multifaceted, and includes the regulation of angiogenesis, body fluid homeostasis, energy metabolism, and functioning of the cardiovascular, nervous, respiratory, digestive, and reproductive systems. This review summarises the mechanism of the apelinergic system in cell apoptosis. Depending on the cell/tissue, the apelinergic system modulates cell apoptosis by activating various signalling pathways, including phosphoinositide 3-kinase (PI3K), extracellular signal-regulated protein kinase (ERK1/2), protein kinase B (AKT), 5’AMP-activated protein kinase(AMPK), and protein kinase A (PKA). Apoptosis is critically important during various developmental processes, and any dysfunction leads to pathological conditions such as cancer, autoimmune diseases, and developmental defects. The purpose of this review is to present data that suggest a significant role of the apelinergic system as a potential agent in various therapies.

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Apelin receptor homodimer inhibits apoptosis in vascular dementia

Cited by 10 publications

References 39 publications

MiR-322-5p Alleviates Cell Injury and Impairment of Cognitive Function in Vascular Dementia by Targeting TSPAN5

MiR-322-5p Alleviates Cell Injury and Impairment of Cognitive Function in Vascular Dementia by Targeting TSPAN5

Neuronal Responses to Ischemia: Scoping Review of Insights from Human-Derived In Vitro Models

The Apelinergic System: Apelin, ELABELA, and APJ Action on Cell Apoptosis: Anti-Apoptotic or Pro-Apoptotic Effect?

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