LINC00938 alleviates hypoxia ischemia encephalopathy induced neonatal brain injury by regulating oxidative stress and inhibiting JNK/p38 MAPK signaling pathway

Zhao, Jing; Le, Meini; Liu, Jie; Huang, Qiong; Chen, H; Zhang, Wenyi; Mao, Huiwen; Sun, Qiang; Li, Aiguo; Zhao, Yanling; Yu, Lingling; M., Yi,; Wang, Jie; Li, Xinyuan; Zhang, Guangming; Ma, Jun; Dong, Xiaohua

doi:10.1016/j.expneurol.2023.114449

Cited by 12 publications

(6 citation statements)

References 37 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…For UHRF2 , a gene set involved in ROS, UV response, and oxidative phosphorylation was induced in the retinal tissue of Uhrf2 deficient mice 47 . Among the 52 PD-linked genes, the majority have established associations with PD and OS (for instances, SLC18A2 48,49 , TXNIP 50 , NEFL 51,52 , MPO 53–56 , LINC00938 57,58 ). Therefore, the 168 OS-PD-DEGs are suggested to include not only well-known OS in PD research candidates, but also novel candidates.…”

Section: Discussionmentioning

confidence: 99%

A systematic exploration of unexploited genes for oxidative stress in Parkinson’s disease

Suzuki,

Bono

2024

Preprint

View full text Add to dashboard Cite

Human disease-associated gene data are accessible through databases, including the Open Targets Platform, DisGeNET, miRTex, RNADisease, and PubChem. However, missing data entries in such databases are anticipated because of factors, such as errors/biases by curators and text mining failures. Additionally, the extensive research on human diseases has resulted in challenges to register comprehensive data. The lack of essential data in databases hinders knowledge sharing and should be addressed. Therefore, we propose an analysis pipeline to explore missing entries of unexploited genes in the human disease-associated gene databases. To demonstrate this, we used the pipeline for genes in Parkinson's disease with oxidative stress, which revealed two unexploited genes: nuclear protein 1 (NUPR1) and ubiquitin-like with PHD and ring finger domains 2 (UHRF2). The proposed methodology and findings facilitate the identification of disease-associated genes that are not completely represented in existing databases, thereby facilitating easier access to the potential human disease-related functional genes.

show abstract

Section: Discussionmentioning

confidence: 99%

A systematic exploration of unexploited genes for oxidative stress in Parkinson’s disease

Suzuki,

Bono

2024

Preprint

View full text Add to dashboard Cite

show abstract

“…As important stress-activated protein kinases, JNK/p38 MAPK are overactivated under intracellular and extracellular stress and followed by the increase in ROS generation and oxidative stress damage, which leads to various forms of cell death like Parthanatos, apoptosis, and ferroptosis (Kwak et al 2021;Liu et al 2023;Zheng et al 2017). Moreover, emerging evidence demonstrated that JNK/p38 MAPK activation involved in many pathological conditions such as neurological disorders and ischemic injury (Zeng et al 2023;Zhang et al 2022a;Zhao et al 2023), where the intracellular context is usually suffered to be attacked by high levels of ROS. We found that exposure to sevo urane resulted in activation of JNK/p38 MAPK in vitro and in vivo, which was paralleled by excess ROS accumulation.…”

Section: Discussionmentioning

confidence: 99%

Sevoflurane exposure triggers ferroptosis of neuronal cells initiated by the activation of ATM/p53 in the neonatal brain via JNK/p38 MAPK-mediated oxidative DNA damage

Gu,

Pan,

Wang

et al. 2024

Preprint

View full text Add to dashboard Cite

The safety of volatile anesthetic exposure in an early life has attracted widespread concern on its potential developmental neurotoxicity. Neuronal death has been regarded as the pivotal pathological factor related to neurotoxic effect caused by volatile anesthetic sevoflurane in the neonatal brain, but the detailed mechanism remains controversial. Ferroptosis is a novel type of regulated cell death driven by excess lipid peroxidation secondary to intracellular iron overload, and implicated in the pathogenesis progression of various neurological disorders. Acting as a death messenger, p53 is mainly activated by ATM during DNA damage, and functions to mediate diverse types of cell death including apoptosis, autophagy and ferroptosis. JNK/p38 MAPK have been proposed important stress-responsive pathways to exacerbate intracellular ROS production, linking DNA damage to many pathological conditions such as neurodegeneration and ischemic injury. Here, we focused on the role of activated ATM/p53-mediated ferroptosis in neuronal death caused by sevoflurane in neonatal brain and elucidated its underlying mechanisms. Our present study demonstrated that sevoflurane exposure-triggered neuronal death was correlated with intracellular iron overload and lipid peroxidation in vitro and in vivo, which was in accordance with the typical features of ferroptosis. Furthermore, we found that neuronal death caused by sevoflurane was associated with ATM/p53 activation in response to DNA damage. Suppressing ATM/p53 pathway counteracted iron-dependent lipid peroxidation, which inhibited neonatal neuronal ferroptosis triggered by sevoflurane. Additionally, sevoflurane exposure resulted in JNK/p38 MAPK activation, followed by intracellular ROS accumulation, leading to DNA damage. Mechanistically, ATM/p53 contributed to neonatal neuronal ferroptosis caused by sevoflurane via two pathways, one is to increase intracellular ferrous iron through upregulating TFR and downregulating FPN, the other is to promote lipid peroxidation via activating NOX4, ALOX12 and ALOX15 and suppressing SLC7A11. Collectively, these findings demonstrated that sevoflurane exposure induced ferroptosis of neuronal cells in the neonatal brain, which was triggered by the ATM/p53 activation via JNK/p38 MAPK-mediated ROS accumulation and resultant DNA damage.

show abstract

“…Western blot analysis was performed as we previously reported ( Dong et al, 2022 ; Zhao et al, 2023a ). Briefly, human dura mater was lysed with Radio Immunoprecipitation Assay (RIPA) lysis buffer (Beyotime, Shanghai, China) which containing 1mM PMSF (Beyotime, Shanghai, China).…”

Section: Methodsmentioning

confidence: 99%

Peptidomics insights: neutrophil extracellular traps (NETs) related to the chronic subdural hemorrhage

Li,

Zhao,

Sun

et al. 2023

PeerJ

Self Cite

View full text Add to dashboard Cite

Chronic subdural hemorrhage (CSDH) refers to a hematoma with an envelope between the dura mater and the arachnoid membrane and is more common among the elderly. It was reported that the dura mater, which is highly vascularized with capillary beds, precapillary arterioles and postcapillary venules play an important role in the protection of the central nervous system (CNS). Numerous evidences suggests that peptides play an important role in neuroprotection of CNS. However, whether dura mater derived endogenous peptides participate in the pathogenesis of CSDH remains undetermined. In the current study, the peptidomic profiles were performed in human dura of CSDH (three patients) and the relative control group (three non-CSDH samples) by LC-MS (liquid chromatography–mass spectrometry). The results suggested that a total of 569 peptides were differentially expressed in the dura matter of CSDH compared with relative controls, including 217 up-regulated peptides and 352 down-regulated peptides. Gene Ontology (GO) analysis demonstrated that the precursor proteins of those differentially expressed peptides were involved in the various biological processes. Interestingly, Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis suggested that NETs participated in the pathogenies of CSDH. Further investigate showed that H3Cit was significantly elevated in the dural and hematoma membranes of patients with CSDH compared to patients without CSDH. Taken together, our results showed the differentially expressed peptides in human dura mater of CSDH and demonstrated that NETs formation in the dural and hematoma membranes might be involved in the pathogenesis of CSDH. It is worth noting that pharmacological inhibition of NETs may have potential therapeutic implications for CSDH.

show abstract

LINC00938 alleviates hypoxia ischemia encephalopathy induced neonatal brain injury by regulating oxidative stress and inhibiting JNK/p38 MAPK signaling pathway

Cited by 12 publications

References 37 publications

A systematic exploration of unexploited genes for oxidative stress in Parkinson’s disease

A systematic exploration of unexploited genes for oxidative stress in Parkinson’s disease

Sevoflurane exposure triggers ferroptosis of neuronal cells initiated by the activation of ATM/p53 in the neonatal brain via JNK/p38 MAPK-mediated oxidative DNA damage

Peptidomics insights: neutrophil extracellular traps (NETs) related to the chronic subdural hemorrhage

Contact Info

Product

Resources

About