Exosomes derived from mesenchyml stem cells ameliorate oxygen-glucose deprivation/reoxygenation-induced neuronal injury via transferring MicroRNA-194 and targeting Bach1

Xu, Li; Zhang, Xin; Liu, Yajun; Pan, Ruihan; Liang, Xiaolong; Huang, Lifa; Yang, Chao

doi:10.1016/j.tice.2021.101651

Cited by 19 publications

(16 citation statements)

References 48 publications

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“…In oxygen-glucose deprivation, miR-194 upregulation improved cell survival and viability, as well as reduced the expression of ACSL4, while upregulating GPX4. These results indicate that miR-194 could potentially reduce ferroptosis and thus improve neuronal survival in vivo (Li et al, 2021d).…”

Section: Ferroptosismentioning

confidence: 73%

miRNA Involvement in Cerebral Ischemia-Reperfusion Injury

et al. 2022

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Cerebral ischemia reperfusion injury is a debilitating medical condition, currently with only a limited amount of therapies aimed at protecting the cerebral parenchyma. Micro RNAs (miRNAs) are small, non-coding RNA molecules that via the RNA-induced silencing complex either degrade or prevent target messenger RNAs from being translated and thus, can modulate the synthesis of target proteins. In the neurological field, miRNAs have been evaluated as potential regulators in brain development processes and pathological events. Following ischemic hypoxic stress, the cellular and molecular events initiated dysregulate different miRNAs, responsible for long-terming progression and extension of neuronal damage. Because of their ability to regulate the synthesis of target proteins, miRNAs emerge as a possible therapeutic strategy in limiting the neuronal damage following a cerebral ischemic event. This review aims to summarize the recent literature evidence of the miRNAs involved in signaling and modulating cerebral ischemia-reperfusion injuries, thus pointing their potential in limiting neuronal damage and repair mechanisms. An in-depth overview of the molecular pathways involved in ischemia reperfusion injury and the involvement of specific miRNAs, could provide future perspectives in the development of neuroprotective agents targeting these specific miRNAs.

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Section: Ferroptosismentioning

confidence: 73%

miRNA Involvement in Cerebral Ischemia-Reperfusion Injury

et al. 2022

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“…The exocrine produced by MSCs cultured in an anoxia and glucose environment had obvious therapeutic effects on brain injury after stroke in rats with transient focal cerebral ischemia [ 31 ]. However, the environment of oxygen and glucose deprivation in the body can lead to endothelial cell and neuronal damage, while MSC-Exos play a protective role in injured endothelium [ 32 ] and through miRNA-194 transfer, they target the Bach1 signal pathway to improve neuronal injury [ 33 ]. HG-HUVEC-Exos induce vascular smooth muscle cell senescence through the circRNA0077930-miR622-KrasCeRNA network, while circRNA-0077930-depleted exosomes lose the ability to promote vascular smooth muscle cell senescence [ 34 ].…”

Section: Blood Glucosementioning

confidence: 99%

Review of the Role of Mesenchymal Stem Cells and Exosomes Derived from Mesenchymal Stem Cells in the Treatment of Orthopedic Disease

2022

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Exosomes can be derived from mesenchymal stem cells (MSCs) and have recently been used to treat defects in the tendons. They may also have applications in treating osteoporosis. MSC-derived exosomes communicate with mesenchymal and osteogenic cells through endocrine or paracrine mechanisms and contribute factors involved in physiological and pathological orthopedic conditions associated with hypoxia and bone tumors. Also, generalized medical conditions, such as obesity, hyperglycemia, and degenerative diseases, can inhibit the osteogenic effect of MSC-derived exosomes. This review aims to present an update on the roles of MSCs and exosomes derived from MSCs in treating orthopedic diseases, such as osteoporosis, and in the repair of cartilage, tendons, and bone fractures.

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“…To further elucidate the effects of miR‐194‐5p on TLE young rats, we down‐regulated the expression of miR‐194‐5p in TLE young rats after GA treatment, and uncovered a reversal of GA‐mediated trends in hippocampal iron content, lipid peroxidation, neuronal injury, and apoptosis. Additionally, the study performed by Li X et al highlighted that exosomal miR‐194 exerts its neuroprotective effects against neuronal injury induced by oxygen–glucose deprivation/reoxygenation 35 . Similarly, Wan et al reported that miR‐194‐5p over‐expression mitigates pathological neuronal injury in rats with intracerebral hemorrhage 36 .…”

Section: Discussionmentioning

confidence: 99%

Glycyrrhizic acid protects against temporal lobe epilepsy in young rats by regulating neuronal ferroptosis through the miR‐194‐5p/PTGS2 axis

Zhang

Huang

2023

The Kaohsiung J of Med Scie

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Temporal lobe epilepsy (TLE) leads to extensive degradation of the quality of life of patients. Glycyrrhizic acid (GA) has been reported to exert neuroprotective effects on status epilepticus. Herein, the current study set out to explore the functional mechanism of GA in TLE young rats. Firstly, TLE young rat models were established using the lithium chloride and pilocarpine regimen and then subjected to treatment with different doses of GA, miR‐194‐5p‐antagomir, or/and sh‐prostaglandin‐endoperoxide synthase 2 (PTGS2) to observe changes in iron content, glutathione and malondialdehyde levels, and GPX4 (glutathione peroxidase 4) and PTGS2 protein levels in the hippocampus. Neuronal injury and apoptosis were assessed through HE, Nissl, and TUNEL staining. Additionally, the expression patterns of miR‐194‐5p were detected. The binding site of miR‐194‐5p and PTGS2 was verified with a dual‐luciferase assay. Briefly, different doses of GA (20, 40, and 60 mg/kg) reduced the epileptic score, frequency, and duration in TLE young rats, along with reductions in iron content, lipid peroxidation, neuronal injury, and apoptosis in the hippocampus. Silencing of miR‐194‐5p partly annulled the action of GA on inhibiting ferroptosis and attenuating neuronal injury in TLE young rats. Additionally, PTGS2 was validated as a target of miR‐194‐5p. GA inhibited ferroptosis and ameliorated neuronal injury in TLE young rats via the miR‐194‐5p/PTGS2 axis. Overall, our findings indicated that GA exerts protective effects on TLE young rats against neuronal injury by inhibiting ferroptosis through the miR‐194‐5p/PTGS2 axis.

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Exosomes derived from mesenchyml stem cells ameliorate oxygen-glucose deprivation/reoxygenation-induced neuronal injury via transferring MicroRNA-194 and targeting Bach1

Cited by 19 publications

References 48 publications

miRNA Involvement in Cerebral Ischemia-Reperfusion Injury

miRNA Involvement in Cerebral Ischemia-Reperfusion Injury

Review of the Role of Mesenchymal Stem Cells and Exosomes Derived from Mesenchymal Stem Cells in the Treatment of Orthopedic Disease

Glycyrrhizic acid protects against temporal lobe epilepsy in young rats by regulating neuronal ferroptosis through the miR‐194‐5p/PTGS2 axis

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