HucMSCs-Derived miR-206-Knockdown Exosomes Contribute to Neuroprotection in Subarachnoid Hemorrhage Induced Early Brain Injury by Targeting BDNF

Zhao, Hao; Li, Yunjun; Chen, Lihua; Shen, Chunsen; Xiao, Zongyu; Xu, Ran; Ji, Wang; Luo, Yongchun

doi:10.1016/j.neuroscience.2019.07.051

Cited by 46 publications

(29 citation statements)

References 51 publications

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“…It was believed that the neuroprotection effect of exosomes on ICH was mainly reflected in the anti-apoptotic effect of miR-133b through mediating RhoA and ERK1/2/CREB signaling pathway (Shen et al, 2018). The MSC-derived miR-206-knockdown exosomes were also confirmed to improve brain edema and neurological deficit in early brain injury of SAH rats, which was probably related to the suppression of neuronal apoptosis via BDNF/TrkB/CREB signaling (Zhao et al, 2019). Except for anti-apoptotic, the effects of neurogenesis and angiogenesis were also observed in the MSCs-derived exosomes treated ICH rats.…”

Section: Exosomes Therapiesmentioning

confidence: 92%

Mesenchymal Stem Cells Transplantation in Intracerebral Hemorrhage: Application and Challenges

Gong

Hao

Wang

2021

Front. Cell. Neurosci.

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Intracerebral hemorrhage (ICH) is one of the leading causes of death and long-term disability worldwide. Mesenchymal stem cell (MSC) therapies have demonstrated improved outcomes for treating ICH-induced neuronal defects, and the neural network reconstruction and neurological function recovery were enhanced in rodent ICH models through the mechanisms of neurogenesis, angiogenesis, anti-inflammation, and anti-apoptosis. However, many key issues associated with the survival, differentiation, and safety of grafted MSCs after ICH remain to be resolved, which hinder the clinical translation of MSC therapy. Herein, we reviewed an overview of the research status of MSC transplantation after ICH in different species including rodents, swine, monkey, and human, and the challenges for MSC-mediated ICH recovery from pathological microenvironment have been summarized. Furthermore, some efficient strategies for the outcome improvement of MSC transplantation were proposed.

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Section: Exosomes Therapiesmentioning

confidence: 92%

Mesenchymal Stem Cells Transplantation in Intracerebral Hemorrhage: Application and Challenges

Gong

Hao

Wang

2021

Front. Cell. Neurosci.

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“…SAH is a devastating disease of the CNS affecting around 22.5 per 100,000 population [68], been associated with high mortality [69]. EBI and cerebral vasospasm are acknowledged as the two major complications after SAH, commonly occurring within 72 h and presenting the main reason behind the poor outcome [70]. Neuroinflammation is considered to be a crucial pathological phenomenon in EBI after SAH [71,72] along with other pathophysiological mechanisms such as elevated ICP, reduced perfusion pressure, disrupted BBB, brain ischemia and edema which may ultimately lead to neuronal injury and death [73].…”

Section: Hmgb1 Mediated Neuroinflammation In Early Brain Injury (Ebi)mentioning

confidence: 99%

HMGB1-Mediated Neuroinflammatory Responses in Brain Injuries: Potential Mechanisms and Therapeutic Opportunities

Paudel

Angelopoulou

Piperi

et al. 2020

IJMS

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Brain injuries are devastating conditions, representing a global cause of mortality and morbidity, with no effective treatment to date. Increased evidence supports the role of neuroinflammation in driving several forms of brain injuries. High mobility group box 1 (HMGB1) protein is a pro-inflammatory-like cytokine with an initiator role in neuroinflammation that has been implicated in Traumatic brain injury (TBI) as well as in early brain injury (EBI) after subarachnoid hemorrhage (SAH). Herein, we discuss the implication of HMGB1-induced neuroinflammatory responses in these brain injuries, mediated through binding to the receptor for advanced glycation end products (RAGE), toll-like receptor4 (TLR4) and other inflammatory mediators. Moreover, we provide evidence on the biomarker potential of HMGB1 and the significance of its nucleocytoplasmic translocation during brain injuries along with the promising neuroprotective effects observed upon HMGB1 inhibition/neutralization in TBI and EBI induced by SAH. Overall, this review addresses the current advances on neuroinflammation driven by HMGB1 in brain injuries indicating a future treatment opportunity that may overcome current therapeutic gaps.

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“…Initially, miR-206 was recognized as a myogenic miRNA since miR-206 is highly expressed in skeletal muscle tissue and actively supports myogenesis when expressed at the right moment, with development of researches, it was reconsidered as a tumor suppressor, inflammatory modulator and functional biomarker for a variety of diseases and disorders (Ma et al, 2015). In the area of neuroprotection, Zhao et al (2019) firstly found that hucMSCs-derived miR-206-knockdown exosomes prevented early brain injury from apoptosis via BDNF/TrkB/CREB signaling in subarachnoid hemorrhage (SAH) rat models (Zhao et al, 2019). Inconsequently, Valsecchi et al (2020) claimed that over-expression of miR-206 exerted an neuroprotective effect on mouse model of spinal muscular atrophy (SMA) via reduction of the predicted target NCX2 which is one of the main regulators of intracellular [Ca2+] and [Na+].…”

Section: Discussionmentioning

confidence: 99%

“…MiR-206 is located on the human chromosome 6p12.2, which is originally thought essential for growth and rebuilding of skeletal muscle (Ma et al, 2015). With the deepening of researches, some studies have shown that miR-206 is also closely involved in regulating ischemia-reperfusion injury (Kong et al, 2019), oxidative stress damage (Ciesla et al, 2016) and neuroprotection (Zhao et al, 2019). Nevertheless, what roles of miR206 act as in the neuronal ischemic hypoxia injury remains to be delved.…”

Section: Introductionmentioning

confidence: 99%

MiR-206 is involved in neuroprotective effects of Dexmedetomidine in H2O2-induced SK-N-SH cells by targeting ANXA1

et al. 2022

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This study focused on exploring the neuroprotective role of Dexmedetomidine (DEX) and miR-206 in H 2 O 2 -induced SK-N-SH cells. First, we dectected the cell viability, apotosis, oxidative stress and miR-206 expression in H 2 O 2 -treated SK-N-SH cells. Next, we examined above content in H 2 O 2 -induced SK-N-SH cells though DEX treatment. Besides, the level of cell viability, apotosis, oxidative stress were evaluated in H 2 O 2 -treated SK-N-SH cells transfected with miR-206 mimics and miR-206 inhibitor. Moreover, the target gene of miR-206 were predicted and verifed by binformatics tools and luciferase reporter assay. These data indicated that H 2 O 2 evoked the apotosis, oxidative stress and inhibition of miR-206 expression in SK-N-SH cells in a dose manner. Besides, DEX attenuated H 2 O 2 -induced oxidative damage, apotosis and promoted miR-206 expression in SK-N-SH cells. Moreover, overexpression of miR-206 augmented the cell viablity as well as suppressed apotosis and oxidative stress in H 2 O 2 -induced SK-N-SH cells, while down-expression of miR-206 showed opppsite effects. Further, Annexin A1 (ANXA1) was verified as a directly target of miR-206, and over-expression of ANXA1 could slack the neuroprotective effect of miR-206 in H 2 O 2 -induced SK-N-SH cells. DEX exerted neuroprotective effects on H 2 O 2 -treated SK-N-SH cells in vitro by negatively reguating ANXA1 expression via activation of miR-206.

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HucMSCs-Derived miR-206-Knockdown Exosomes Contribute to Neuroprotection in Subarachnoid Hemorrhage Induced Early Brain Injury by Targeting BDNF

Cited by 46 publications

References 51 publications

Mesenchymal Stem Cells Transplantation in Intracerebral Hemorrhage: Application and Challenges

Mesenchymal Stem Cells Transplantation in Intracerebral Hemorrhage: Application and Challenges

HMGB1-Mediated Neuroinflammatory Responses in Brain Injuries: Potential Mechanisms and Therapeutic Opportunities

MiR-206 is involved in neuroprotective effects of Dexmedetomidine in H2O2-induced SK-N-SH cells by targeting ANXA1

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