lnc-MRGPRF-6:1 Promotes M1 Polarization of Macrophage and Inflammatory Response through the TLR4-MyD88-MAPK Pathway

Hu, Dan; Wang, Yu‐Zhong; You, Zhihuan; Lu, Yuan-Qiang; Liang, Caihong

doi:10.1155/2022/6979117

Cited by 9 publications

(6 citation statements)

References 32 publications

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“…It was reported that the injury of macrophages in AS was associated with ferroptosis [ 32 ]. In our previous study, it was demonstrated that lnc-MRGPRF-6:1 was highly expressed in CAD patients and could mediate macrophage polarization to promote inflammation progression in AS [ 5 ]. In the present study, it was demonstrated that ox-LDL-induced macrophage ferroptosis and lnc-MRGPRF-6:1 could promote ox-LDL-induced macrophage ferroptosis in AS.…”

Section: Discussionmentioning

confidence: 99%

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lnc-MRGPRF-6:1 Promotes ox-LDL-Induced Macrophage Ferroptosis via Suppressing GPX4

You,

Ye,

Jiang

et al. 2023

Mediators of Inflammation

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Background. Ferroptosis, a newly discovered mode of cell death, emerges as a new target for atherosclerosis (AS). Long noncoding RNAs (lncRNAs) are involved in the regulation of ferroptosis. In our previous study, lnc-MRGPRF-6:1 was highly expressed in patients with coronary atherosclerotic disease (CAD) and closely associated with macrophage-mediated inflammation in AS. In the present study, we aim to investigate the role of lnc-MRGPRF-6:1 in oxidized-low-density lipoprotein (ox-LDL)-induced macrophage ferroptosis in AS. Methods. Firstly, ox-LDL-treated macrophages were used to simulate macrophage injury in AS. Then, ferroptosis-related biomarkers and mitochondrial morphology were detected and observed in ox-LDL-treated macrophages. Subsequently, we constructed lnc-MRGPRF-6:1 knockdown and overexpression of THP-1-derived macrophages and investigated the role of lnc-MRGPRF-6:1 in ox-LDL-induced ferroptosis. Then human monocytes were isolated successfully and were used to explore the role of lnc-MRGPRF-6:1 in macrophage ferroptosis. Likely, we constructed lnc-MRGPRF-6:1 knockdown and overexpression of human monocyte-derived macrophages and detected the expression levels of ferroptosis-related biomarkers. Then, transcriptome sequencing, literature searching, and following quantitative real-time polymerase chain reaction and western blot were implemented to explore specific signaling pathway in the process. It was demonstrated that lnc-MRGPRF-6:1 may regulate ox-LDL-induced macrophage ferroptosis through glutathione peroxidase 4 (GPX4). Eventually, the correlation between lnc-MRGPRF-6:1 and GPX4 was measured in monocyte-derived macrophages of CAD patients and controls. Results. The ox-LDL-induced injury in macrophages was involved in ferroptosis. The knockdown of lnc-MRGPRF-6:1 could alleviate ox-LDL-induced ferroptosis in macrophages. Meanwhile, the overexpression of lnc-MRGPRF-6:1 could intensify ox-LDL-induced ferroptosis. Furthermore, the knockdown of lnc-MRGPRF-6:1 could alleviate the decrease of GPX4 induced by RAS-selective lethal compounds 3 (RSL-3). These indicated that lnc-MRGPRF-6:1 may suppress GPX4 to induce macrophage ferroptosis. Eventually, lnc-MRGPRF-6:1 was highly expressed in the monocyte-derived macrophages of CAD patients and was negatively correlated with the expression of GPX4. Conclusion. lnc-MRGPRF-6:1 can promote ox-LDL-induced macrophage ferroptosis through inhibiting GPX4.

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Section: Discussionmentioning

confidence: 99%

“…As is known to all, inflammatory progression is essential basis of AS [ 4 ]. Macrophage-mediated inflammation plays an important role in the pathophysiology of AS [ 5 ]. The progression of inflammation is closely associated with cell death [ 6 ].…”

Section: Introductionmentioning

confidence: 99%

lnc-MRGPRF-6:1 Promotes ox-LDL-Induced Macrophage Ferroptosis via Suppressing GPX4

You,

Ye,

Jiang

et al. 2023

Mediators of Inflammation

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“…Many studies have indicated that exosomes can be used as carriers of lncRNA to regulate cellular activities of neighboring cells. The upregulation of lnc-MRGPRF-6:1 expression and as its correlation with levels of proinflammatory mediators have been detected in the plasma exosomes of patients with CAD [67]. The expression level of lnc-MRGPRF-6:1 following M1 induction was higher than that following M2 induction in THP-1 cells.…”

Section: Lncrnas Functioning Via Exosomes In Atherogenesismentioning

confidence: 97%

Role of Macrophage lncRNAs in Mediating Inflammatory Processes in Atherosclerosis and Sepsis

Shin

Park

et al. 2023

Biomedicines

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Long noncoding RNAs (lncRNAs) are molecules >200 bases in length without protein-coding functions implicated in signal transduction and gene expression regulation via interaction with proteins or RNAs, exhibiting various functions. The expression of lncRNAs has been detected in many cell types, including macrophages, a type of immune cell involved in acute and chronic inflammation, removal of dead or damaged cells, and tissue repair. Increasing evidence indicates that lncRNAs play essential roles in macrophage functions and disease development. Additionally, many animal studies have reported that blockage or modulation of lncRNA functions alleviates disease severity or morbidity rate. The present review summarizes the current knowledge regarding lncRNAs expressed in macrophages, focusing on their molecular targets and the biological processes regulated by them during the development of inflammatory diseases such as atherosclerosis and sepsis. Possible application of this information to lncRNA-targeting therapy is also discussed. The studies regarding macrophage lncRNAs described in this review can help provide valuable information for developing treatments for various pathological conditions involving macrophages.

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“…For example, EV’s resealed by endothelial progenitor cells promote M2 macrophage polarization by suppressing miR-9-5p on SIRT1 through the transfer on lncRNA taurine upregulated gene 1 (TUG1), an important lncRNA that is downregulated during sepsis ( 44 ). In patients with coronary atherosclerosis, EVs carrying lncRNA-MRGPRF-6:1 promote M1 macrophage polarization by activating TLR4, myeloid differentiation factor-8, and mitogen-activated protein kinase (TLR4-MyD88-MAPK) ( 45 ). Also, blockade of lnc-RNA-ASLNCS5088-enriched EVs dampens the effect of M2 macrophages in fibroblast activation ( 46 ).…”

Section: Potential Interactions Of Extracellular Vesicles and Immune ...mentioning

confidence: 99%

Immunometabolism, extracellular vesicles and cardiac injury

Omoto,

do Carmo,

da Silva

et al. 2024

Front. Endocrinol.

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Recent evidence from our lab and others suggests that metabolic reprogramming of immune cells drives changes in immune cell phenotypes along the inflammatory-to-reparative spectrum and plays a critical role in mediating the inflammatory responses to cardiac injury (e.g. hypertension, myocardial infarction). However, the factors that drive metabolic reprogramming in immune cells are not fully understood. Extracellular vesicles (EVs) are recognized for their ability to transfer cargo such as microRNAs from remote sites to influence cardiac remodeling. Furthermore, conditions such as obesity and metabolic syndrome, which are implicated in the majority of cardiovascular disease (CVD) cases, can skew production of EVs toward pro-inflammatory phenotypes. In this mini-review, we discuss the mechanisms by which EVs may influence immune cell metabolism during cardiac injury and factors associated with obesity and the metabolic syndrome that can disrupt normal EV function. We also discuss potential sources of cardio-protective and anti-inflammatory EVs, such as brown adipose tissue. Finally, we discuss implications for future therapeutics.

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lnc-MRGPRF-6:1 Promotes M1 Polarization of Macrophage and Inflammatory Response through the TLR4-MyD88-MAPK Pathway

Cited by 9 publications

References 32 publications

lnc-MRGPRF-6:1 Promotes ox-LDL-Induced Macrophage Ferroptosis via Suppressing GPX4

lnc-MRGPRF-6:1 Promotes ox-LDL-Induced Macrophage Ferroptosis via Suppressing GPX4

Role of Macrophage lncRNAs in Mediating Inflammatory Processes in Atherosclerosis and Sepsis

Immunometabolism, extracellular vesicles and cardiac injury

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