&lt;p&gt;LncRNA MEG3 Reduces Hippocampal Neuron Apoptosis via the PI3K/AKT/mTOR Pathway in a Rat Model of Temporal Lobe Epilepsy&lt;/p&gt;

Zhang, Hongyan; Tao, Jiuyun; Zhang, Shuxia; Lv, Xinxin

doi:10.2147/ndt.s270614

Cited by 23 publications

(20 citation statements)

References 33 publications

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“…For instance, CDKN2B-AS1 was reported to up-regulate the expression of GDNF and inhibit neuronal apoptosis by acting as the molecular sponge for miR-133 ( Jiang et al, 2021 ). In addition, the expression of MEG3 was down-regulated in rats with TLE, and overexpression of MEG3 reduced the release of proinflammatory cytokines (including IL-1β, IL-6, and TNF-α) and inhibited neuronal apoptosis via the PI3K/AKT/mTOR pathway in the hippocampus ( Zhang et al, 2020 ). UBA6-AS1 might regulate cell proliferation and apoptosis by competitively binding to miR-7648 and targeting YTHDC1 ( Zheng et al, 2021 ).…”

Section: Discussionmentioning

confidence: 99%

Study of Neuronal Apoptosis ceRNA Network in Hippocampal Sclerosis of Human Temporal Lobe Epilepsy by RNA-Seq

Wang

et al. 2021

Front. Neurosci.

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Hippocampal sclerosis (HS) is one of the most common pathological type of intractable temporal lobe epilepsy (TLE), often characterized by hippocampal atrophy, neuronal apoptosis, and gliogenesis. However, the molecular mechanisms of neuronal apoptosis in patients with HS are still not fully understood. We therefore conducted a pilot study focusing on the neuronal apoptosis ceRNA network in the sclerotic hippocampus of intractable TLE patients. In this research, RNA sequencing (RNA-seq) was utilized to quantify the expression levels of lncRNAs, miRNAs, and mRNAs in TLE patients with HS (HS-TLE) and without HS (non-HS-TLE), and reverse transcription-quantitative PCR (qRT-PCR). The interactions of differential expression (DE) lncRNAs-miRNAs or DEmiRNAs-mRNAs were integrated by StarBase v3.0, and visualized using Cytoscape. Subsequently, we annotate the functions of lncRNA-associated competitive endogenous RNA (ceRNA) network through analysis of their interactions with mRNAs. RNA-seq analyses showed 381 lncRNAs, 42 miRNAs, and 457 mRNAs were dysregulated expression in HS-TLE compared to non-HS-TLE. According to the ceRNA hypothesis, 5 HS-specific ceRNA network were constructed. Among them, the core ceRNA regulatory network involved in neuronal apoptosis was constituted by 10 DElncRNAs (CDKN2B-AS1, MEG3, UBA6-AS1, etc.), 7 DEmiRNAs (hsa-miR-155-5p, hsa-miR-195-5p, hsa-miR-200c-3p, etc.), and 3 DEmRNAs (SCN2A, DYRK2, and MAPK8), which belonging to apoptotic and epileptic terms. Our findings established the first ceRNA network of lncRNA-mediated neuronal apoptosis in HS-TLE based on transcriptome sequencing, which provide a new perspective on the disease pathogenesis and precise treatments of HS.

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Section: Discussionmentioning

confidence: 99%

Study of Neuronal Apoptosis ceRNA Network in Hippocampal Sclerosis of Human Temporal Lobe Epilepsy by RNA-Seq

Wang

et al. 2021

Front. Neurosci.

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“…AKT, also known as protein kinase B, is an important targeted kinase downstream of PI3K. This pathway is closely related to neuronal survival because many neurotrophic factors play a protective role in the brain by activating the pathway, thus inhibiting apoptosis [ 22 ]. Similar to our findings, a previous study showed that dexmedetomidine improved propofol-induced neuronal injury in rat hippocampus through the PI3K/Akt pathway [ 23 ].…”

Section: Discussionmentioning

confidence: 99%

Protective effect of Houttuynia cordata extract on propofol-induced injury of rat hippocampal neurons by regulating PI3K/Akt and Toll-like receptor 4/NF-κB signaling pathway

2021

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Objective This study was to detect the protective effects of Houttuynia cordata extract on the damage induced by propofol in hippocampal neuron of rats. Methods Propofol-induced neuron injury model and H. cordata extract administration were conducted. Immunofluorescence and immunoblot were conducted for the effect of H. cordata extract on neuronal activity and inflammation were detected in this model. Results H. cordata extracts increased neuronal activity, and reduced propofol-induced neuronal inflammation levels. H. cordata extract also reduced propofol-induced neuronal apoptosis. Mechanically, we noticed H. cordata extract activated phosphoinositide 3-kinase/AKT pathway and suppressed Toll-like receptor 4/nuclear factor kappaB pathway, therefore protected propofol-induced injury of rat hippocampal neurons. Conclusion Our findings provide references for anesthetic use in infants and young children.

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“…Lithium induces Bcl-2 transcription in retinas. Bcl-2 is a main controller for the regulation of both neural survival and axonal regeneration [ 131 ]. Moreover, the mechanism of Bcl-2 control of apoptosis [ 132 ].…”

Section: Lithium and Aaps In Glaucomamentioning

confidence: 99%

Lithium and Atypical Antipsychotics: The Possible WNT/β Pathway Target in Glaucoma

Vallée

Lecarpentier³

2021

Biomedicines

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Glaucoma is a progressive neurodegenerative disease that represents the major cause of irreversible blindness. Recent findings have shown which oxidative stress, inflammation, and glutamatergic pathway have main roles in the causes of glaucoma. Lithium is the major commonly used drug for the therapy of chronic mental illness. Lithium therapeutic mechanisms remain complex, including several pathways and gene expression, such as neurotransmitter and receptors, circadian modulation, ion transport, and signal transduction processes. Recent studies have shown that the benefits of lithium extend beyond just the therapy of mood. Neuroprotection against excitotoxicity or brain damages are other actions of lithium. Moreover, recent findings have investigated the role of lithium in glaucoma. The combination of lithium and atypical antipsychotics (AAPs) has been the main common choice for the treatment of bipolar disorder. Due to the possible side effects gradually introduced in therapy. Currently, no studies have focused on the possible actions of AAPs in glaucoma. Recent studies have shown a down regulation of the WNT/β-catenin pathway in glaucoma, associated with the overactivation of the GSK-3β signaling. The WNT/β-catenin pathway is mainly associated with oxidative stress, inflammation and glutamatergic pathway. Lithium is correlated with upregulation the WNT/β-catenin pathway and downregulation of the GSK-3β activity. Thus, this review focuses on the possible actions of lithium and AAPs, as possible therapeutic strategies, on glaucoma and some of the presumed mechanisms by which these drugs provide their possible benefit properties through the WNT/β-catenin pathway.

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<p>LncRNA MEG3 Reduces Hippocampal Neuron Apoptosis via the PI3K/AKT/mTOR Pathway in a Rat Model of Temporal Lobe Epilepsy</p>

Cited by 23 publications

References 33 publications

Study of Neuronal Apoptosis ceRNA Network in Hippocampal Sclerosis of Human Temporal Lobe Epilepsy by RNA-Seq

Study of Neuronal Apoptosis ceRNA Network in Hippocampal Sclerosis of Human Temporal Lobe Epilepsy by RNA-Seq

Protective effect of Houttuynia cordata extract on propofol-induced injury of rat hippocampal neurons by regulating PI3K/Akt and Toll-like receptor 4/NF-κB signaling pathway

Lithium and Atypical Antipsychotics: The Possible WNT/β Pathway Target in Glaucoma

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