miRNA-124-3p targeting of LPIN1 attenuates inflammation and apoptosis in aged male rats cardiopulmonary bypass model of perioperative neurocognitive disorders

Han, Jiang; Pu, Cui-Xia; Xiao, Qiu‐Xia; Lin, Ting; Liu, Ting; He, Li; Ren, Ying-Bo; Liu, Qing; Zhang, Ying

doi:10.1016/j.exger.2021.111578

Cited by 13 publications

(4 citation statements)

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“…The bioinformatic analysis allowed us to identify that LPIN1 is a critical gene in sepsis. In addition, the in vitro and in vivo studies verified that LPS stimulation could inhibit the expression of LPIN1 with the facilitation of TNFα, TLR4, IKK, p65 subunit, and IκB ( 29 ).…”

Section: Discussionmentioning

confidence: 92%

LPIN1 Is a Regulatory Factor Associated With Immune Response and Inflammation in Sepsis

et al. 2022

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ObjectivesSepsis is a clinical disease that is typically treated in the intensive care unit, and the complex pathophysiology under this disease has not been thoroughly understood. While ferroptosis is involved in inflammation and infection, its effect in sepsis is still unknown. The study aimed to identify ferroptosis-related genes in sepsis, providing translational potential therapeutic targets.MethodsThe dataset GSE65682 was used to download the sample source from the Gene Expression Omnibus (GEO) database. Consensus weighted gene co-expression network analysis (WGCNA) was performed to find suspected modules of sepsis. The differentially expressed genes (DEGs) most significantly associated with mortality were intersected with those altered by lipopolysaccharide (LPS) treatment and were further analyzed for the identification of main pathways of Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis. The related pathway markers were further verified by qPCR.ResultsA total of 802 blood samples with sepsis were included for WGCNA, which identified 21 modules. Intersected with ferroptosis databases and LPS treatment groups, we identified two ferroptosis-related genes: PEBP1 and LPIN1. Only LPIN1 contributes to a poor outcome. Then, 205 DEGs were further identified according to the high or low LPIN1 expression. Among them, we constructed a gene regulatory network with several transcriptional factors using the NetworkAnalyst online tool and identified that these genes mostly correlate with inflammation and immune response. The immune infiltration analysis showed that lower expression of LPIN1 was related to macrophage infiltration and could be an independent predictor factor of the survival status in sepsis patients. Meanwhile, the multivariate Cox analysis showed that LPIN1 had a significant correlation with survival that was further verified by in vitro and in vivo experiments.ConclusionIn conclusion, LPIN1 could become a reliable biomarker for patient survival in sepsis, which is associated with immune and inflammation status.

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Section: Discussionmentioning

confidence: 92%

LPIN1 Is a Regulatory Factor Associated With Immune Response and Inflammation in Sepsis

et al. 2022

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“…In another study, miR-124-3p was found to be reduced in the perioperative neurocognitive disorder (PND) rat model after a cardiopulmonary bypass (CPB) procedure, and its overexpression showed a protective effect against PND by alleviating cognitive decline, inflammation, and cell apoptosis. Additionally, miR-124-3p was predicted to directly target LPIN1, suggesting a potential therapeutic strategy for preventing and treating PND [185].…”

Section: Mir-124-3pmentioning

confidence: 99%

Epigenetic Alterations of Cognition Functions in Parkinson's Disease

Hasani,

Ahmadi,

Masrour

et al. 2024

Preprint

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The field of epigenetics, which explores how heritable traits or stable alterations of cell functions occur without changes to the DNA sequence and how environmental factors affect gene expression, is rapidly advancing. Epigenetics plays a critical role in memory formation, learning, and cognitive functioning, effectively bridging genetics with environmental influence. Maternal behavior in rats, for instance, can modify the stress response of their offspring through epigenetic mechanisms such as histone acetylation and DNA methylation. Understanding neurodegenerative diseases like Parkinson's disease (PD) depends on comprehending the mechanisms of epigenetic regulation. Epigenetic modifications, which alter proteins and DNA structure without changing the DNA sequence, can activate or suppress gene expression, assisting organisms in adapting to environmental changes. These modifications may influence genes involved in inflammation, synaptic plasticity, and neuroprotection, potentially contributing to cognitive deficits in PD patients. MicroRNAs (miRNAs), histone modifications, and DNA methylation are the epigenetic mechanisms that significantly influence cell differentiation and maintain normal cellular activity. Understanding the intricate molecular processes of epigenetics could lead to more targeted and effective therapies. Despite numerous findings on how epigenetics affects cognitive alterations in PD patients, only some studies coordinate and integrate these results. Here, we summarize recent findings on how epigenetic changes impact gene expression linked to cognitive impairments in PD.

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“…Among these miRNAs, miRNA-124 is an essential posttranscriptional regulator of in ammatory genes expression [12,13]. It has been shown in several models of in ammatory diseases that miRNA-124 modulates the expression of their in ammatory target genes and participates in the regulation of in ammatory responses [14][15][16]. Qin et al have made a comprehensive review of the role of this miRNA in the immune system and in ammatory diseases, which emphasizes the essential role of this miRNA in regulating immune system activities [17].…”

Section: Introductionmentioning

confidence: 99%

The effects of nicotine on microRNA-124 expression in the bile duct ligation- induced liver fibrosis in rats

Hajiasgharzadeh,

Shahabi,

Karimi-Sales

et al. 2023

Preprint

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Background Smoking causes a variety of adverse effects on organs that have no direct contact with the smoke itself such as the liver. Nicotine as a main compound of smoking may exert its effects by changing the expression of microRNAs (miRNAs). This study was conducted to further investigate the molecular mechanisms of miRNA-dependent effects of nicotine in an animal model of liver fibrosis. Methods First, the bile duct ligation (BDL) approach was used in male Wistar rats to create a model of liver fibrosis. Then, the effects of nicotine administration on miRNA-124 expression, as well as fibrosis and inflammation-related genes were investigated using the quantitative Real-Time PCR method. The total bilirubin and liver enzymes activity levels were measured using the colorimetric assay. Also, the effects of nicotine on the process of liver fibrosis were investigated with histological studies. Results The development of liver fibrosis in BDL rats leads to a decrease in miRNA-124 expression. Also, a decrease in miRNA-124 expression has been seen in the groups administered nicotine. The decrease in the expression of miRNA-124 is accompanied by the increase in the expression of fibrotic and proinflammatory genes. Also, the significant increase in bilirubin and liver enzymes in fibrotic rats worsens with nicotine administration. The results of histological studies also confirm these results. Conclusion Considering that miRNA-124 is an anti-inflammatory miRNA, it can be concluded that the decrease in its expression due to nicotine exposure leads to an increase in inflammatory processes and subsequently to an increase in liver fibrosis.

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miRNA-124-3p targeting of LPIN1 attenuates inflammation and apoptosis in aged male rats cardiopulmonary bypass model of perioperative neurocognitive disorders

Cited by 13 publications

References 50 publications

LPIN1 Is a Regulatory Factor Associated With Immune Response and Inflammation in Sepsis

LPIN1 Is a Regulatory Factor Associated With Immune Response and Inflammation in Sepsis

Epigenetic Alterations of Cognition Functions in Parkinson's Disease

The effects of nicotine on microRNA-124 expression in the bile duct ligation- induced liver fibrosis in rats

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