WTAP mediates the anti-inflammatory effect of Astragalus mongholicus polysaccharide on THP-1 macrophages

Long, Haijiao; Lin, Haiyue; Zheng, Ping; Hou, Lianjie; Zhang, Ming; Lin, Shuyun; Yin, Kedong; Zhao, Guo-Jun

doi:10.3389/fphar.2022.1023878

Cited by 12 publications

(7 citation statements)

References 20 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…WTAP mediated the m6A modification of NLRP3 mRNA, and WTAP mRNA levels were positively correlated with pro‐inflammatory cytokines and NLRP3 inflammasome 25 . Long et al 26 confirmed that astragalus mongholicus polysaccharides exerted anti‐inflammatory effect by reducing WTAP‐mediated m6A modification in THP‐1 macrophages. To sum up, differential m6A methylation of WTAP may play a pro‐inflammatory role by upregulating its mRNA expression in our study.…”

Section: Discussionmentioning

confidence: 95%

Changes in N6‐methyladenosine RNA methylomes of human periodontal ligament cells in response to inflammatory conditions

Zou

Liu

et al. 2023

J of Periodontal Research

View full text Add to dashboard Cite

Objective To investigate the changes in the m6A methylation modification profile of human periodontal ligament cells (hPDLCs) in response to inflammatory conditions. Background Periodontitis is an infectious disease of the periodontal support tissue that leads to the loss of alveolar bone. HPDLCs are primary cells that can repair periodontal tissue defects caused by periodontitis. However, the inflammatory conditions induce inflammatory damage and decrease ossification of hPDLCs. This inflammatory response depends on genetic and epigenetic mechanisms, including m6A methylation. Methods HPDLCs were cultured with osteogenic induction medium (NC group), while TNF‐α (10 ng/mL) and IL‐1β (5 ng/mL) were added to simulate inflammatory conditions (Inflam group). Then RNA‐seq and MeRIP‐seq analyses were performed to identify m6A methylation modification in the transcriptome range of hPDLCs. Results The results showed that the osteogenic differentiation of hPDLCs was inhibited under inflammatory conditions. RNA‐seq analysis also revealed that the decreased genes in response to inflammatory conditions were primarily annotated in processes associated with ossification. Compared with the NC group, differentially m6A‐methylated genes were primarily enriched in histone modification processes. Among 145 histone modification genes, 25 genes have been reported to be involved in the regulation of osteogenic differentiation, and they include KAT6B, EP300, BMI1, and KDMs (KDM1A, KDM2A, KDM3A, KDM4B, and KDM5A). Conclusion This study demonstrated that the m6A landscape of hPDLCs was changed in response to inflammation. M6A methylation differences among histone modification genes may act on the osteogenic differentiation of hPDLCs.

show abstract

Section: Discussionmentioning

confidence: 95%

Changes in N6‐methyladenosine RNA methylomes of human periodontal ligament cells in response to inflammatory conditions

Zou

Liu

et al. 2023

J of Periodontal Research

View full text Add to dashboard Cite

show abstract

“…Research has shown that m6A may have clinical benefits in the management of AS. WTAP regulates m6A modification expression in THP-1 macrophages [42] to exert anti-inflammatory effect of APS. WTAP mediated the injurious effects of myocardial I/R by augmenting cell apoptosis and ER stress through a mechanisms involving the modulation of m6A modification on ATF4 mRNA [43] .…”

Section: Discussionmentioning

confidence: 99%

The role of m6A methyltransferase WTAP in inflammatory response of atherosclerosis through NF-κB/NLRP3 mediated pyroptosis

Hu,

He,

Sha

et al. 2024

Preprint

View full text Add to dashboard Cite

Background: Pyroptosis is a new form of pro-inflammatory programmed cell death that has been linked to the development of atherosclerosis (AS). However, its exact mechanisms are not known. N6-methyladenosine (m6A) methylation is the commonest and most abundant epigenetic modification of eukaryotic mRNAs. m6A methylation modulates pathological and physiological processes involved in cardiovascular diseases. However, the exact mechanism by which it regulates inflammation in AS is unclear. Methods: In this study, the level of m6A and WTAP in CHD was explored. To determine the effect of WTAP on the release of pyrolysis-related proteins and pro-inflammatory cytokines, the expression of WTAP in lipopolysaccharide (LPS)-treated endothelial cells was silenced. Pyroptosis-related proteins and pro-inflammatory cytokines were quantified in the presence of NLRP3 shRNA (shNLRP3) and NF-kB shRNA (shNF-kB(p50)). The interaction of NF-kB and NLRP3 was examined through immunoprecipitation (CO-IP), immunofluorescence (IF) and GST-pull down assays. Result: It was observed that lipopolysaccharide (LPS) induced Nod-like receptor protein 3 (NLRP3)-mediated pyroptosis and inflammation, both of which were abolished through the knockdown of WTAP. Interestingly, our results indicated that WTAP enhanced the function of nuclear factor κB (NF-κB) p50 (an NF-κB subunit) and that p50 could interact with NLRP3 in endothelial cells. Conclusion: In conclusion, these results suggested that WTAP in the formation of pyroptosis and inflammation in endothelial cells exposed to LPS stress by activating the NF-κB/NLRP3 signaling pathway. These findings demonstrate the mechanism of WTAP regulation during the progression of AS.

show abstract

“…It has several bio-activities, including anti-inflammatory, proliferative, and immune-regulating effects, and a molecular weight of 3.6 × 10 4 Da ( Sun et al, 2021a ). Studies have demonstrated that APS significantly abrogates LPS-induced IL-6 levels in THP-1 macrophages ( Long et al, 2022 ). ABCA1 expression in foam cells exposed to TNF-α increases in response to APS ( Wang et al, 2010a ).…”

Section: Antiatherosclerotic Herbal Medicine Potentially Targeting Tr...mentioning

confidence: 99%

Trained immunity in monocyte/macrophage: Novel mechanism of phytochemicals in the treatment of atherosclerotic cardiovascular disease

Wang

Liu²,

Hu³

et al. 2023

Front. Pharmacol.

View full text Add to dashboard Cite

Atherosclerosis (AS) is the pathology of atherosclerotic cardiovascular diseases (ASCVD), characterized by persistent chronic inflammation in the vessel wall, in which monocytes/macrophages play a key role. It has been reported that innate immune system cells can assume a persistent proinflammatory state after short stimulation with endogenous atherogenic stimuli. The pathogenesis of AS can be influenced by this persistent hyperactivation of the innate immune system, which is termed trained immunity. Trained immunity has also been implicated as a key pathological mechanism, leading to persistent chronic inflammation in AS. Trained immunity is mediated via epigenetic and metabolic reprogramming and occurs in mature innate immune cells and their bone marrow progenitors. Natural products are promising candidates for novel pharmacological agents that can be used to prevent or treat cardiovascular diseases (CVD). A variety of natural products and agents exhibiting antiatherosclerotic abilities have been reported to potentially interfere with the pharmacological targets of trained immunity. This review describes in as much detail as possible the mechanisms involved in trained immunity and how phytochemicals of this process inhibit AS by affecting trained monocytes/macrophages.

show abstract

WTAP mediates the anti-inflammatory effect of Astragalus mongholicus polysaccharide on THP-1 macrophages

Cited by 12 publications

References 20 publications

Changes in N6‐methyladenosine RNA methylomes of human periodontal ligament cells in response to inflammatory conditions

Changes in N6‐methyladenosine RNA methylomes of human periodontal ligament cells in response to inflammatory conditions

The role of m6A methyltransferase WTAP in inflammatory response of atherosclerosis through NF-κB/NLRP3 mediated pyroptosis

Trained immunity in monocyte/macrophage: Novel mechanism of phytochemicals in the treatment of atherosclerotic cardiovascular disease

Contact Info

Product

Resources

About