Potential new therapeutic intervention for ischemic stroke

Wu, Jang‐Yen; Prentice, Howard

doi:10.2478/jtim-2021-0014

Cited by 5 publications

(5 citation statements)

References 11 publications

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“…Growing evidence demonstrated that the overproduction of reactive oxygen species (ROS), mitochondrial damage, neuroinflammation, and abnormal homocysteine metabolism are crucial for the development of neurological diseases, such as ischemic stroke and cognitive impairment [6][7][8][9][10]. It was reported that ferroptosis could participate in oxidative stress response, mitochondrial dysfunction, neuroinflammation, and abnormal homocysteine metabolism [11][12][13].…”

Section: Introductionmentioning

confidence: 99%

Mesenchymal Stem Cell-Derived Exosomes Ameliorate Delayed Neurocognitive Recovery in Aged Mice by Inhibiting Hippocampus Ferroptosis via Activating SIRT1/Nrf2/HO-1 Signaling Pathway

Liu

Huang

Zhang

et al. 2022

Oxidative Medicine and Cellular Longevity

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Delayed neurocognitive recovery (dNCR) is a prevalent perioperative neurological complication in older patients and has common characteristics such as acute cognitive dysfunction, impaired memory, and inattention. Mesenchymal stem cell-derived exosomes (MSCs-Exo) are enclosed by a lipid bilayer contain proteins, DNA, miRNA, and other components, which are important mediators of intercellular communication. It has been reported that exosomes could play an important role in the treatment of neurodegenerative diseases, nerve injury, and other neurological diseases. In this study, we examined the effects of MSCs-Exo on dNCR aged mice after exploratory laparotomy and evaluated their potential regulatory mechanisms. We found that MSCs-Exo treatment ameliorated cognitive impairment in dNCR aged mice. MSCs-Exo inhibit hippocampus ferroptosis and increase the expression of silent information regulator 1 (SIRT1), factor nuclear factor-erythroid 2-related factor 2 (Nrf2), and heme oxygenase-1 (HO-1) in dNCR aged mice. Interestingly, the above effects of MSCs-Exo on dNCR aged mice were abolished by SIRT1 selective inhibitor EX-527. In conclusion, these findings indicated that MSCs-Exo can ameliorate cognitive impairment by inhibiting hippocampus ferroptosis in dNCR aged mice via activating SIRT1/Nrf2/HO-1 signaling pathway, providing a potential avenue for the treatment of dNCR.

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Section: Introductionmentioning

confidence: 99%

Mesenchymal Stem Cell-Derived Exosomes Ameliorate Delayed Neurocognitive Recovery in Aged Mice by Inhibiting Hippocampus Ferroptosis via Activating SIRT1/Nrf2/HO-1 Signaling Pathway

Liu

Huang

Zhang

et al. 2022

Oxidative Medicine and Cellular Longevity

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“…Li et al reported that miR-335 enhances ferroptosis in vitro and in vivo models of Parkinson’s disease by degrading FTH1 (Xinrong Li et al, 2021). The pathogenesis of stroke is complex and is thought to potentially be related to glutamate-induced oxidative stress ( Wu and Prentice, 2021 ). It was confirmed that exosomal miR-137 can inhibit oxyhemoglobin-induced ferroptosis in SH-SY5Y cells, thereby initiating protection ( Li et al, 2020 ).…”

Section: Introductionmentioning

confidence: 99%

The role of microRNAs in ferroptosis

Guo

Zhang²,

Liu³

2022

Front. Mol. Biosci.

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Ferroptosis is a newly discovered type of programmed cell death, which is closely related to the imbalance of iron metabolism and oxidative stress. Ferroptosis has become an important research topic in the fields of cardiomyopathy, tumors, neuronal injury disorders, and ischemia perfusion disorders. As an important part of non-coding RNA, microRNAs regulate various metabolic pathways in the human body at the post-transcriptional level and play a crucial role in the occurrence and development of many diseases. The present review introduces the mechanisms of ferroptosis and describes the relevant pathways by which microRNAs affect cardiomyopathy, tumors, neuronal injury disorders and ischemia perfusion disorders through regulating ferroptosis. In addition, it provides important insights into ferroptosis-related microRNAs, aiming to uncover new methods for treatment of the above diseases, and discusses new ideas for the implementation of possible microRNA-based ferroptosis-targeted therapies in the future.

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“…Even after survival, many individuals require costly medical care and suffer from disabilities for the remainder of their lifetimes (Wolf & Ergul, 2021 ). Different techniques have been studied to potentially mitigate these morbidities (Wu & Prentice, 2021 ). Conditioning strategies are reported to play a key role in reducing injury as well as improving functional outcomes in stroke patients (Basalay et al., 2020 ; Li et al., 2020 ).…”

Section: Introductionmentioning

confidence: 99%

Exercise postconditioning reduces ischemic injury via suppression of cerebral gluconeogenesis in rats

Ilagan

et al. 2022

Brain and Behavior

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Pre‐stroke exercise conditioning reduces neurovascular injury and improves functional outcomes after stroke. The goal of this study was to explore if post‐stroke exercise conditioning (PostE) reduced brain injury and whether it was associated with the regulation of gluconeogenesis. Adult rats received 2 h of middle cerebral artery (MCA) occlusion, followed by 24 h of reperfusion. Treadmill activity was then initiated 24 h after reperfusion for PostE. The severity of the brain damage was determined by infarct volume, apoptotic cell death, and neurological deficit at one and three days after reperfusion. We measured gluconeogenesis including oxaloacetate (OAA), phosphoenolpyruvate (PEP), pyruvic acid, lactate, ROS, and glucose via ELISA, as well as the location and expression of the key enzyme phosphoenolpyruvate carboxykinase (PCK)‐1/2 via immunofluorescence. We also determined upstream pathways including forkhead transcription factor (FoxO1), p‐FoxO1, 3‐kinase (PI3K)/Akt, and p‐PI3K/Akt via Western blot. Additionally, the cytoplasmic expression of p‐FoxO1 was detected by immunofluorescence. Compared to non‐exercise control, PostE (*p < .05) decreased brain infarct volumes, neurological deficits, and cell death at one and three days. PostE groups (*p < .05) saw increases in OAA and decreases in PEP, pyruvic acid, lactate, ROS, glucose levels, and tissue PCKs expression on both days. PCK‐1/2 expressions were also significantly (*p < .05) suppressed by the exercise setting. Additionally, phosphorylated PI3K, AKT, and FoxO1 protein expression were significantly induced by PostE at one and three days (*p < .05). In this study, PostE reduced brain injury after stroke, in association with activated PI3K/AKT/FoxO1 signaling, and inhibited gluconeogenesis. These results suggest the involvement of FoxO1 regulation of gluconeogenesis underlying post‐stroke neuroprotection.

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Potential new therapeutic intervention for ischemic stroke

Cited by 5 publications

References 11 publications

Mesenchymal Stem Cell-Derived Exosomes Ameliorate Delayed Neurocognitive Recovery in Aged Mice by Inhibiting Hippocampus Ferroptosis via Activating SIRT1/Nrf2/HO-1 Signaling Pathway

Mesenchymal Stem Cell-Derived Exosomes Ameliorate Delayed Neurocognitive Recovery in Aged Mice by Inhibiting Hippocampus Ferroptosis via Activating SIRT1/Nrf2/HO-1 Signaling Pathway

The role of microRNAs in ferroptosis

Exercise postconditioning reduces ischemic injury via suppression of cerebral gluconeogenesis in rats

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