MicroRNA-23b alleviates neuroinflammation and brain injury in intracerebral hemorrhage by targeting inositol polyphosphate multikinase

Hu, Liuting; Zhang, Heyu; Wang, Bingyang; Ao, Qiang; Shi, Jing; He, Zhiwei

doi:10.1016/j.intimp.2019.105887

Cited by 32 publications

(29 citation statements)

References 52 publications

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“…Sara Negrini et al confirmed that p75 NTR has a positive regulatory role in the control of mTOR complex 2 activity in PC12-27 cells [34]. Down-regulation of the mTOR pathway has been suggested to mediate cell autophagy and lead to less inflammation following ICH [35]. As quite similar to our findings, mTOR signal activation has been revealed to participate in the pathophysiological process during ICH, and rapamycin-induced mTOR inactivation has been suggested to reduce the levels of IL-1β, IL-6, TNF-α, and caspase 3 in the following ICH [36].…”

Section: Discussionmentioning

confidence: 98%

RETRACTED ARTICLE: Role of p75 neurotrophin receptor in neuronal autophagy in intracerebral hemorrhage in rats through the mTOR signaling pathway

2020

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Rupture of weakened blood vessels could lead to severe intracerebral hemorrhage (ICH) and brain injuries. This study was designed to explore the roles of p75 neurotrophin receptor (p75 NTR) in neuronal autophagy in ICH rats. An ICH rat model was established, and then gain and loss of functions of p75 NTR in rat tissues were performed. Then, the pathologic morphology, water content, and inflammation in brain tissues were assessed. Western blot analysis was applied to detect the levels of inflammatory proteins, apoptosis-and autophagy-related proteins, and the mammalian target of rapamycin (mTOR) pathwayrelated proteins. Neuronal autophagy was further measured with mTOR activated. In vitro experiments were also performed on brain microvascular endothelial cells (BMECs) and astrocytes. Consequently, we found p75 NTR knockdown improved the pathologic morphology with reduced neuron damage, water content, permeability of blood-brain barrier and inflammation in ICH rat brain tissues. Besides, Knockdown of p75 NTR decreased neuronal apoptosis and inactivated mTOR signaling pathway, but it elevated the levels of autophagy-related proteins. In vivo results were reproduced in in vitro experiments. This study demonstrated that knockdown of p75 NTR could promote neuronal autophagy and reduce neuronal apoptosis via inactivating the mTOR pathway. We hope these findings could provide new therapeutic options for ICH treatment.

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Section: Discussionmentioning

confidence: 98%

RETRACTED ARTICLE: Role of p75 neurotrophin receptor in neuronal autophagy in intracerebral hemorrhage in rats through the mTOR signaling pathway

2020

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“…We noted an inverse correlation between manic symptoms and level of serum miR-23b. Additionally, miR-23b was reported to be downregulated in patients with intracerebral haemorrhages 42 , and an animal study indicated that overexpression of miR-23b in the brain may alleviate neurological functional deficits in rats, possibly due to its anti-inflammatory effects, by modulating neuroinflammation and neuronal protection 43 . Because inflammation may be an etiology for manic symptom, whether miR-23b may be a state marker for manic symptoms merits investigation.…”

Section: Discussionmentioning

confidence: 99%

Serum miRNA as a possible biomarker in the diagnosis of bipolar II disorder

Lee

Wang

et al. 2020

Sci Rep

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The diagnosis of Bipolar II disorder (BD-II) is currently based on the patients' description of symptoms and clinical behavioral observations. This study explored the possibility of miRNA in peripheral blood (serum) as a specific biomarker for BD-II. We identified 6 candidate miRNAs to differentiate BD-II patients from controls using next-generation sequencing. We then examined these candidate miRNAs using real-time PCR in the first cohort (as training group) of 79 BD-II and 95 controls. A diagnostic model was built based on these candidate miRNAs and then tested on an individual testing group (BD-II: n = 20, controls: n = 20). We found that serum expression levels of miR-7-5p, miR-23b-3p, miR-142-3p, miR-221-5p, and miR-370-3p significantly increased in BD-II compared with controls in the first cohort, whereas that of miR-145-5p showed no significant difference. The diagnostic power of the identified miRNAs was further analyzed using receiver-operating characteristic (ROC). Support vector machine (SVM) measurements revealed that a combination of the significant miRNAs reached good diagnostic accuracy (AUC: 0.907). We further examined an independent testing group and the diagnostic power reached fair for BD-II (specificity = 90%, sensitivity = 85%). We constructed miRNA panels using SVM model, which may aid in the diagnosis for BD-II.Bipolar disorder (BD) has several subtypes. Bipolar I disorder (BD-I) and bipolar II disorder (BD-II) are two of the most commonly seen subtypes of BD. BD-I and BD-II differ in clinical presentation: BD-I involves one or more manic or mixed episodes in addition to one or more major depressive episodes. BD-II is characterised by at least one hypomanic episode with one or more major depressive episodes 1,2 . BD-II has become the focus of increasing attention and has been recognised as a unique disorder. Its prevalence rate ranges from 3% to 11% 3 . Nevertheless, because of the complex spectrum of symptoms, the diagnosis of BD remains subjective. Diagnosing BD is challenging because patients typically regard hypomanic episodes as a positive mood status or experience, and they only seek medical help during depressive episodes 4 . BD is initially misdiagnosed at a rate of approximately 40% and typically requires approximately 5-12 years to be correctly diagnosed and treated appropriately 5,6 . Delayed diagnosis and inefficacious treatment of BD-II may lead to a prolonged course, more affective episodes, and an increased suicide rate, adding further to its socioeconomic burden 5,7 .Accumulating evidence reveals that microribonucleic acids (miRNAs) are involved in many biological processes such as neurogenesis, neuroproliferation, and synaptic plasticity in the central nervous system 8,9 . Different expressions of peripheral miRNA have been reported in several mental disorders including schizophrenia, major depressive disorder, and Alzheimer disease [10][11][12] . Changes in peripheral miRNA may be correlated with changes in neuroendocrine or neuroimmune responses 13 . Because brain tissue ...

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“…This evidence suggested the anti-inflammatory effect of miR-340-5p on ICH-induced brain injury in vivo. miRNAs have been reported to function in response to human diseases by regulating the downstream target gene levels [21,24]. In the present study, PDCD4 was identified to be a target gene of miR-340-5p in microglial cells.…”

Section: Pdcd4 Was a Direct Target Gene Of Mir-340-5pmentioning

confidence: 51%

“…Considering this evidence, the accurate role and underlying mechanism of miR-340-5p in ICH attract our interest. Currently, the collagenase-induced model is widely used as a prevalent animal model to better mimic human ICH syndrome [21,22]. In the present study, the collagenase-induced ICH rat model was established to investigate the role of miR-340-5p in ICH-induced brain injury in vitro.…”

Section: Pdcd4 Was a Direct Target Gene Of Mir-340-5pmentioning

confidence: 99%

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

Zhou

Huang

et al. 2020

Cerebrovasc Dis

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Objective: Intracerebral hemorrhage (ICH) is a common cerebrovascular disease. Increasing evidence has documented the crucial role of microRNAs in ICH. The present study aimed to investigate the role and underlying mechanism of miR-340-5p in ICH. Methods: The collagenase-induced ICH rat model was established. The neurological function of rats and the cerebral water content of rat brain tissue were measured to assess the brain injury. BV-2 cells were recruited and treated by LPS to mimic ICH-induced inflammatory response. qRT-PCR was used for the measurement of miR-340-5p. The protein levels of TNF-α, IL-6, and IL-1β were detected using ELISA. Luciferase reporter gene assay was performed to confirm the target gene. Results: Downregulation of miR-340-5p was detected in the serum of ICH patients and the brain tissues of ICH rats. Overexpression of miR-340-5p reversed the influence of ICH on the neurological function score and cerebral water content and inhibited the production of proinflammatory cytokines (TNF-α, IL-6, and IL-1β), which were induced by ICH in vivo. In in vitro study, levels of TNF-α, IL-6, and IL-1β were significantly enhanced in cells after LPS treatment, but these increases were eliminated by overexpression of miR-340-5p. PDCD4 was a direct target gene of miR-340-5p. Conclusion: miR-340-5p protects against brain injury after ICH. miR-340-5p might exert an anti-inflammatory effect during the occurrence of ICH via targeting PDCD4.

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MicroRNA-23b alleviates neuroinflammation and brain injury in intracerebral hemorrhage by targeting inositol polyphosphate multikinase

Cited by 32 publications

References 52 publications

RETRACTED ARTICLE: Role of p75 neurotrophin receptor in neuronal autophagy in intracerebral hemorrhage in rats through the mTOR signaling pathway

RETRACTED ARTICLE: Role of p75 neurotrophin receptor in neuronal autophagy in intracerebral hemorrhage in rats through the mTOR signaling pathway

Serum miRNA as a possible biomarker in the diagnosis of bipolar II disorder

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

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