Reduced SULT2B1b expression alleviates ox-LDL-induced inflammation by upregulating miR-148-3P via inhibiting the IKKβ/NF-κB pathway in macrophages

Yin, Mengzhuo; Lu, Jianwen; Guo, Zhaoze; Zhang, Yanan; Liu, Jichen; Wu, Tong; Guo, Kai; Luo, Tao

doi:10.18632/aging.202273

Cited by 11 publications

(6 citation statements)

References 42 publications

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“…The relationship between p38, MSK1, and NF-kB pathways has already been reported during inflammation, as well as the effects of inhibitors or the knockdown of target genes [52,53]. Consistent with previous data reporting that upregulated miR-148a-3p reduced the expression of inflammatory mediators such as MSK1 and NF-κB in different experimental models [17,54], we found decreased NF-κB and activated MSK1 protein levels in miR-148a-transfected cells exposed to IL-6 stress. Our in vitro data suggest that MSK1 may serve as a noteworthy target of miR-148a-3p, resulting in a decrease in NF-kB.…”

Section: Discussionsupporting

confidence: 90%

“…MiR-148a-3p, belonging to the miR-148/152 family [12], modulates endothelial cell function by affecting lipid metabolism and contributing to chronic syndromes [13]. MiR-148a-3p may oppose endothelial dysfunction by promoting proliferation and migration, and by inhibiting apoptosis via FOXO3 and FOXO4 [14], and it is able to attenuate inflammation, functional injury, and apoptosis in human umbilical vein endothelial cells (HUVECs) and macrophages [15][16][17]. Contrasting evidence reported the capacity of miR-148a-3p to promote M1 macrophage polarization and enhance inflammation via Notch signaling in septic mice [18].…”

Section: Introductionmentioning

confidence: 99%

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MiR-148a-3p/SIRT7 Axis Relieves Inflammatory-Induced Endothelial Dysfunction

Anastasio,

Donisi,

Colloca

et al. 2024

IJMS

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In endothelial cells, miR-148a-3p is involved in several pathological pathways, including chronic inflammatory conditions. However, the molecular mechanism of miR-148a-3p in endothelial inflammatory states is, to date, not fully elucidated. To this end, we investigated the involvement of miR-148a-3p in mitochondrial dysfunction and cell death pathways in human aortic endothelial cells (teloHAECs) treated with interleukin-6 (IL-6), a major driver of vascular dysfunction. The results showed that during IL6-activated inflammatory pathways, including increased protein levels of sirtuin 7 (SIRT7) (p < 0.01), mitochondrial stress (p < 0.001), and apoptosis (p < 0.01), a decreased expression of miR-148a-3p was observed (p < 0.01). The employment of a miR-148a mimic counteracted the IL-6-induced cytokine release (p < 0.01) and apoptotic cell death (p < 0.01), and ameliorated mitochondria redox homeostasis and respiration (p < 0.01). The targeted relationship between miR-148a-3p and SIRT7 was predicted by a bioinformatics database analysis and validated via the dual-luciferase reporter assay. Mechanistically, miR-148a-3p targets the 3′ untranslated regions of SIRT7 mRNA, downregulating its expression (p < 0.01). Herein, these in vitro results support the role of the miR-148a-3p/SIRT7 axis in counteracting mitochondrial damage and apoptosis during endothelial inflammation, unveiling a novel target for future strategies to prevent endothelial dysfunction.

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Section: Discussionsupporting

confidence: 90%

Section: Introductionmentioning

confidence: 99%

MiR-148a-3p/SIRT7 Axis Relieves Inflammatory-Induced Endothelial Dysfunction

Anastasio,

Donisi,

Colloca

et al. 2024

IJMS

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“…Recent studies have found that miR-148a-3p plays a critical role in inflammatory diseases (27)(28)(29) and angiogenesis (30,31). The knockdown of SULT2B1b has been shown to inhibit the inflammatory response via increasing the miR-148a-3p level in macrophages (32). Moreover, CNTN4 was reported to be associated with the development of cardiovascular events (33).…”

Section: Mir-148a-3p Attenuates Apoptosis and Inflammation By Targeti...mentioning

confidence: 99%

MiR-148a-3p attenuates apoptosis and inflammation by targeting CNTN4 in atherosclerosis

Wang¹,

Huang²,

Miao³

et al. 2022

Ann Transl Med

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Background: Atherosclerosis (AS) seriously affects human health. The role of microRNAs (miRNAs) in the pathogenesis and progression of AS has become a focus of research. Our goal was to identify the biological effect of differentially expressed miRNAs (DE-miRNAs) in AS. Methods:To analyze differentially expressed genes (DEGs), including differentially expressed mRNAs (DE-mRNAs) and DE-miRNAs, in AS by using the Gene Expression Omnibus (GEO) database and limma package. DEGs protein-protein interaction (PPI) network and functional enrichment analysis were constructed by using the search tool for the retrieval of interacting genes/proteins (STRING) database, Cytoscape software and Cytoscape plugin "ClueGO2.5.6". We established a coexpression network of dysregulated miRNAs and mRNAs to predict the function of miRNAs by using miRWalk database and Pearson correlation coefficient (PCC) analysis. Cellular experiments were used to validate the results of bioinformatics.Results: First, 69 common DEGs were obtained from datasets GSE43292 and GSE97210 using the limma package in R. Next, a DEG PPI network was constructed. Functional enrichment analysis of DEGs showed that 11 functional pathways were significantly enriched, such as positive regulation of monocyte chemotaxis.Seven common DE-miRNAs were obtained from the GSE99685 dataset and DE-mRNAs predicted miRNAs through the miRWalk database. The miRNA-mRNA network constructed using Cytoscape software suggested that miR-148a-3p targeted contactin 4 (CNTN4). Quantitative real-time polymerase chain reaction (qRT-PCR) assay results indicated that miR-148a-3p was downregulated and CNTN4 was upregulated in the THP-1 + phorbol 12-myristate 13-acetate (PMA) + oxidized low-density lipoprotein (oxLDL) group compared with the THP-1 + PMA group. qRT-PCR, flow cytometry, and ELISA found that upregulated miR-148a-3p significantly inhibited the expression of CNTN4, cell apoptosis, and interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α) concentrations in oxLDL-induced THP-1 macrophages. In addition, a dual-luciferase reporter assay demonstrated that CNTN4 was a target gene of miR-148a-3p.Conclusions: Overall, these findings suggested that miR-148a-3p inhibited oxLDL-induced cell apoptosis and inflammation via targeting CNTN4 in THP-1 macrophages.

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“…no. 20605ES05; Shanghai Yeasen Biotechnology Co., Ltd.) for 48 h to induce the formation of foam cells ( 18 , 19 ).…”

Section: Methodsmentioning

confidence: 99%

Inhibition of miR-200b-3p alleviates lipid accumulation and promotes cholesterol efflux by targeting ABCA1 in macrophage-derived foam cells

Wu¹,

Li²,

Lin³

et al. 2021

Exp Ther Med

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Atherosclerosis (As) is a chronic cardiovascular disease characterized by abnormal of lipid accumulation and cholesterol efflux. The present study aimed to investigate whether the micro-RNA (miR)-200b-3p could exacerbate As by promoting lipid accumulation and inhibiting cholesterol efflux via ATP-binding cassette transporter A1 (ABCA1) in macrophage-derived foam cells. Blood samples from 30 patients with As and 30 healthy people were collected at Quanzhou First Hospital. RAW264.7 cells were used to establish foam cells using oxidized low-density lipoprotein. The expression of miR-200b-3p and ABCA1 was evaluated by reverse transcription quantitative PCR and western blotting. Lipid accumulation was analyzed by Oil Red O staining and cholesterol content was assessed by ELISA. A targeting relationship between miR-200b-3p and ABCA1 was demonstrated by luciferase reporter assays. Compared with healthy volunteers and RAW264.7 cells, the expression level of miR-200b-3p was significantly increased whereas the expression level of ABCA1 was significantly decreased in patients with As and foam cells. Furthermore, miR-200b-3p expression was negatively correlated with ABCA1 expression in the blood of the patients with As. Lipid content was significantly decreased and cholesterol efflux was significantly increased in foam cells transfected with the miR-200b-3p inhibitor compared with inhibitor control cells. In addition, ABCA1 was shown to be targeted by miR-200b-3p. Furthermore, the lipid content in foam cells transfected with the miR-200b-3p inhibitor and small interfering-ABCA1 was significantly increased, while the cholesterol efflux was significantly decreased compared with foam cells transfected with the miR-200b-3p inhibitor. In conclusion, the findings from the present study indicated that inhibition of miR-200b-3p may alleviate lipid accumulation and promote cholesterol efflux by targeting ABCA1 in macrophage-derived foam cells.

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Reduced SULT2B1b expression alleviates ox-LDL-induced inflammation by upregulating miR-148-3P via inhibiting the IKKβ/NF-κB pathway in macrophages

Cited by 11 publications

References 42 publications

MiR-148a-3p/SIRT7 Axis Relieves Inflammatory-Induced Endothelial Dysfunction

MiR-148a-3p/SIRT7 Axis Relieves Inflammatory-Induced Endothelial Dysfunction

MiR-148a-3p attenuates apoptosis and inflammation by targeting CNTN4 in atherosclerosis

Inhibition of miR-200b-3p alleviates lipid accumulation and promotes cholesterol efflux by targeting ABCA1 in macrophage-derived foam cells

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