Protective Effect of miR-340-5p against Brain Injury after Intracerebral Hemorrhage by Targeting PDCD4

Zhou, Wei; Huang, Guandong; Ye, Jueming; Jiang, Jiamei; Xu, Qing

doi:10.1159/000508210

Cited by 14 publications

(6 citation statements)

References 30 publications

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“…It has been reported that miR‐340‐5p mitigates oxygen‐glucose deprivation/reoxygenation‐induced neuronal injury through targeting neuronal differentiation 4 (Zheng et al., 2020 ). Additionally, miR‐340‐5p targets PDCD4 to reduce inflammatory response and ameliorate intracerebral hemorrhage‐induced brain injury (Zhou et al., 2020 ). Also, miR‐340‐5p mitigates spinal cord injury‐induced neuroinflammation and neuronal apoptosis via modulating the p38‐MAPK signaling pathway (Qian et al., 2020 ).…”

Section: Discussionmentioning

confidence: 99%

“…Also, many miRNAs, such as miR‐124 and miR‐193b‐3p, are also found to be dysregulated during the pathogenesis of SAH (Chen et al., 2020 ; Lai et al., 2020 ). Reportedly, miR‐340‐5p can reduce cerebral hemorrhage and spinal cord injury‐induced nerve injury and play a protective role by inhibiting neuroinflammation (Qian et al., 2020 ; Zhou et al., 2020 ), but its expression and function in SAH have not been reported yet.…”

Section: Introductionmentioning

confidence: 99%

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MiR‐340‐5p alleviates neuroinflammation and neuronal injury via suppressing STING in subarachnoid hemorrhage

Song

2022

Brain and Behavior

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Background: Subarachnoid hemorrhage (SAH) is a severe acute neurological disorder.SAH causes neuroinflammation and leads to early brain injury (EBI) and secondary injury. MicroRNAs are crucial regulators in a variety of neurological diseases. This study was performed to decipher how miR-340-5p functions in SAH.Methods: An experimental mouse model with SAH was established by the intravascular perforation, and the in vitro SAH model was constructed by exposing cocultured primary neurons and microglia to oxyhemoglobin. After overexpression of miR-340-5p in mice, the neurobehavioral disorders were evaluated by Garcia test; brain edema was evaluated by wet-dry method; blood-brain barrier (BBB) damage was detected with Evan's blue staining; levels of inflammatory cytokines were detected with enzymelinked immunosorbent assay. After miR-340-5p was transfected in to microglia, Iba-1 expression was detected by Western blot, and neuronal apoptosis were detected with flow cytometry. The targeting relationship between miR-340-5p and STING was verified by dual-luciferase reporter gene assay and RNA immunoprecipitation assay.Results: MiR-340-5p was significantly inhibited in the brain tissues of mice with SAH and microglia of SAH model, and neurological impairment, brain edema, BBB injury, and neuroinflammation were significantly alleviated in mice after overexpressing miR-340-5p. STING was identified as a target of miR-340-5p, and STING overexpression could counteract the effects of miR-340-5p overexpression on neurons. Conclusion:MiR-340-5p can attenuate EBI caused by SAH-induced neuroinflammation by inhibiting STING.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

MiR‐340‐5p alleviates neuroinflammation and neuronal injury via suppressing STING in subarachnoid hemorrhage

Song

2022

Brain and Behavior

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“…To explore the mechanism of baicalein on brain injury after ICH, we established a model of brain injury after ICH by collagenase induction, and then ICH model was treated by baicalein. Neural function and brain tissue water content are widely used to evaluate the degree of brain injury after ICH [25]. The results showed that after baicalein treatment, nervous system damage, lesion volume and brain water content were decreased, cell apoptosis was decreased, the number of Nissl bodies was increased, and pathological severity signi cantly was decreased.…”

Section: Discussionmentioning

confidence: 99%

Mechanism of Baicalein in Brain Injury After Intracerebral Hemorrhage by Inhibiting the ROS/NLRP3 Inflammasome Pathway

et al. 2021

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Intracerebral hemorrhage (ICH) is a devastating subtype of stroke with high disability/mortality. Baicalein has strong anti-in ammatory activity. This study aims to explore the mechanism of baicalein on brain injury after ICH. The model of brain injury after ICH was established by collagenase induction, followed by the evaluation of neurological severity, brain water content, the degenerated neurons, neuronal apoptosis and reactive oxygen species (ROS). The ICH model was treated with baicalein and silencing NLRP3 to detect brain injury. The expression of NLRP3 in ammasome was detected after treatment with ROS scavenger. The expression of oxidative stress markers and in ammatory factors were detected, and the levels of components in NLRP3 in ammasome were detected. Baicalein reduced the damage of nervous system, lesion surface, brain water content and apoptosis. Baicalein inhibited malondialdehyde and increased IL-10 by inhibiting ROS in brain tissue after ICH. Baicalein inhibited the high expression of NLRP3 in ammasome in ICH. ROS scavenger inhibited the NLRP3 in ammatory response by inhibiting ROS levels. Silencing NLRP3 alleviated the brain injury after ICH by inhibiting excessive oxidative stress and in ammatory factors. Overall, baicalein alleviated the brain injury after ICH by inhibiting ROS and NLRP3 in ammasome.

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“…miRNA played an important role in a series of key biological processes, including cell proliferation, differentiation and metabolism [21]. Numbers of miRNAs have been revealed play crucial roles in intracerebral hemorrhage, such as miR-124, miR-340-5p and miR-26a-5p [22][23][24]. However, there was less studies focus on HICH regulated by miRNAs.…”

Section: Discussionmentioning

confidence: 99%

miR-20a-5p/RBM24 Axis Alleviated Hypertensive Intracerebral Hemorrhage via Regulating HIF1α/VEGFA Signaling Pathway

Xu¹,

Mo²,

Lü³

et al. 2021

Preprint

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Background: Hypertensive intracerebral hemorrhage presented high incidence and high mortality owing to its difficult to diagnose. However, the molecular mechanism of HICH remains unclear. Therefore, this study aims to investigate the key miRNAs and the mechanism of the key miRNAs in HICH. Methods: miRNAs chip was used to explore the differentially expressed miRNAs in HICH patients. In vitro and in vivo HICH models were established by Ang-II. Cell Counting Kit-8 (CCK8), flow cytometry, transwell assay and tube formation analysis were used to detect cell proliferation, apoptosis, cell migration and tube formation, respectively. Hematoxylin-eosin staining was used to evaluate the intracerebral hemorrhage in vivo HICH model. The regulatory mechanism of miR-20a-5p in HICH was confirmed by dual luciferase reporter assay, immunofluorescence, qRT-PCR, western blot and rescue experiments. Results: miR-20a-5p showed the most downregulated in HICH patients compared with healthy individuals and significantly associated with clinicopathological characteristics of HICH. Upregulation of miR-20a-5p promoted cell proliferation, migration and tube formation while inhibited apoptosis in vitro and ameliorated the development of HICH in vivo. RBM24 is a direct target of miR-20a-5p and silencing RBM24 could partially recovery the development of HICH caused by miR-20a-5p inhibition both in vivo and in vitro. miR-20a-5p regulated the development of HICH depending on HIF1α/VEGFA pathway. Conclusion: Our results demonstrated that miR-20a-5p/RBM24 axis regulated hypertensive intracerebral hemorrhage via regulating HIF1α/VEGFA signaling pathway, in support of further investigation into miR-20a-5p therapies for HICH treatment.

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Protective Effect of miR-340-5p against Brain Injury after Intracerebral Hemorrhage by Targeting PDCD4

Cited by 14 publications

References 30 publications

MiR‐340‐5p alleviates neuroinflammation and neuronal injury via suppressing STING in subarachnoid hemorrhage

MiR‐340‐5p alleviates neuroinflammation and neuronal injury via suppressing STING in subarachnoid hemorrhage

Mechanism of Baicalein in Brain Injury After Intracerebral Hemorrhage by Inhibiting the ROS/NLRP3 Inflammasome Pathway

miR-20a-5p/RBM24 Axis Alleviated Hypertensive Intracerebral Hemorrhage via Regulating HIF1α/VEGFA Signaling Pathway

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