Functioning of Long Noncoding RNAs Expressed in Macrophage in the Development of Atherosclerosis

Ma, Xirui; Liu, Huifang; Chen, Fengling

doi:10.3389/fphar.2020.567582

Cited by 6 publications

(4 citation statements)

References 118 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Previous studies have revealed the potential atherogenic role of GAS5 through its upregulation in endothelial cells and macrophages following ox-LDL stimulation [ 13 , 36 ]. GAS5 knockdown suppressed apoptosis, inflammation, and cholesterol efflux in ox-LDL treated THP-1 cells [ 16 , 17 , 37 , 38 ].…”

Section: Discussionmentioning

confidence: 99%

The lncRNA GAS5 upregulates ANXA2 to mediate the macrophage inflammatory response during atherosclerosis development

Xue,

Hu,

et al. 2024

Heliyon

View full text Add to dashboard Cite

Section: Discussionmentioning

confidence: 99%

The lncRNA GAS5 upregulates ANXA2 to mediate the macrophage inflammatory response during atherosclerosis development

Xue,

Hu,

et al. 2024

Heliyon

View full text Add to dashboard Cite

“…Enhanced phagocytosis improves lipid uptake and foam cell formation, enables lesion formation, which is protective in the early stage of atherosclerosis [ 31 ]. In advanced atherosclerosis, incomplete clearance and defective phagocytosis give rise to necrotic cores, which might contribute to plaque instability and plaque rupture [ 44 ]. Thus, further in vivo studies are needed to determine whether miR-185-5p plays diverse role in different stages of atherosclerosis.…”

Section: Discussionmentioning

confidence: 99%

miR-185-5p Regulates Inflammation and Phagocytosis through CDC42/JNK Pathway in Macrophages

Liu

Zhu

et al. 2022

Genes

Self Cite

View full text Add to dashboard Cite

Macrophage activation is an essential component of systemic chronic inflammation and chronic inflammatory diseases. Emerging evidence implicates miR-185-5p in chronic inflammation diseases. However, the regulatory role of miR-185-5p in macrophage pro-inflammatory activation has not been studied previously. Here, we identified that miR-185-5p was one of the top genes and effectively downregulated in two macrophage miRNA expression datasets from GEO. Under LPS stress, miR-185-5p overexpression reduced pro-inflammatory cytokine expression, suppressed phagocytosis in RAW264.7 macrophage. miR-185-5p inhibitors augmented pro-inflammatory effects of LPS in macrophage. Mechanically, miR-185-5p sponged and negatively regulated the protein expression of CDC42. Ablation of CDC42 with selective CDC42 inhibitor CASIN reversed the pro-inflammatory effect of miR-185-5p inhibitors through inhibiting MAPK/JNK pathways. Collectively, these data demonstrate that miR-185-5p exhibited anti-inflammatory functions in LPS-induced RAW264.7 macrophages at least partially through CDC42/JNK pathways. Our findings yield insights into the understanding of miR-185-5p-regulated network in macrophages inflammation, which is beneficial for exploring miRNA-protein interaction in atherosclerotic inflammation.

show abstract

“…LncRNA-Mirt2 inhibits the NF-κB and MAPK pathways activation and limits the production of pro-in ammatory cytokines through negative feedback 38 . In addition, lncRNAs can participate in in ammatory progression by regulating macrophage oxidative stress and metabolism 39,40 . Our study found that LINC01126 silencing signi cantly reduced expression of proin ammatory cytokines in LPS-induced HGFs, particularly IL-6.…”

Section: Discussionmentioning

confidence: 99%

Long non-coding RNA 01126 activates IL-6/JAK2/STAT3 pathway via serving as a sponge of miR-655-3p in periodontitis

Tang¹,

Li²,

Yu³

et al. 2021

Preprint

View full text Add to dashboard Cite

Background Periodontitis is a serious threat to oral quality of life and overall health. Although our previous studies confirmed that long intergenic non-coding RNA 01126 (LINC01126) is aberrantly expressed in periodontitis tissues, there are few reports on the pathogenesis of LINC01126 in periodontitis. Our study investigated the biological functions of LINC01126 in periodontitis and the potential mechanism. Results An inflammatory model of human gingival fibroblasts (HGFs) was successfully established. LINC01126 silencing can alleviate lipopolysaccharide (LPS) induced cell inflammation, reduce cell apoptosis, and promote cell migration. As a "sponge" for miR-655-3p, LINC01126 inhibits its binding to mRNA of IL-6, thereby promoting inflammation progression and JAK2/STAT3 pathway activation. qRT- PCR, WB, and IHC results of clinical tissue samples further confirmed that miR-655-3p expression was down-regulated and IL-6/JAK/STAT3 was abnormally activated in periodontitis tissues. Conclusions Our results indicate that LINC01126, as an endogenous competitive RNA (ceRNA) of miR-655-3p, can promote IL-6/JAK3/STAT3 pathway activation, thereby promoting periodontitis pathogenesis. And this is the first study of miR-655-3p in inflammatory periodontal diseases. Our study reveales a new pathogenesis of periodontitis, and provides a new strategy for preventing and treating periodontitis.

show abstract

Functioning of Long Noncoding RNAs Expressed in Macrophage in the Development of Atherosclerosis

Cited by 6 publications

References 118 publications

The lncRNA GAS5 upregulates ANXA2 to mediate the macrophage inflammatory response during atherosclerosis development

The lncRNA GAS5 upregulates ANXA2 to mediate the macrophage inflammatory response during atherosclerosis development

miR-185-5p Regulates Inflammation and Phagocytosis through CDC42/JNK Pathway in Macrophages

Long non-coding RNA 01126 activates IL-6/JAK2/STAT3 pathway via serving as a sponge of miR-655-3p in periodontitis

Contact Info

Product

Resources

About