Long noncoding RNAs and atherosclerosis

Zhou, Tian; Ding, Jiawang; Wang, Xinan; Zheng, Xia-Xia

doi:10.1016/j.atherosclerosis.2016.02.025

Cited by 81 publications

(63 citation statements)

References 124 publications

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“…ABCA1 and ABCG1 deficiency increased inflammatory cytokine production via activation of TLR4 signaling in macrophages (42). In addition, ABCA1 and ABCG1 suppress macrophage inflammatory responses through activation of TLR2 and TLR3 (9,43,44). Activation of TLR3 and TLR4 signaling suppresses expression of ABCA1 and ABCG1 in macrophages (43,44).…”

Section: Macrophage Receptors Involved In Lipid Accumulation and Inflmentioning

confidence: 99%

“…Macrophages with high cholesterol accumulation can induce chronic inflammation, which facilitates the development of foam cells and atherosclerotic plaques. Many lncRNAs have been identified in atherosclerotic plaques or ox-LDL-induced macrophage-derived foam cells (9). Several lncRNAs are involved in the regulation of cholesterol metabolism and inflammation (61, 62), which might unveil the molecular mechanism of cholesterol-mediated inflammation (Table 1, Figure 1).…”

Section: Lncrna Biology and Function In Atherosclerosismentioning

confidence: 99%

“…Recently, several lncRNAs that interfere with the progress of atherosclerosis have been identified. They also participate in the pathology of atherosclerosis such as EC dysfunction, cholesterol accumulation, and inflammation (9). For example, lncRNAgrowth arrest-specific 5 (GAS5) expression was significantly increased in the atherosclerotic plaque and exaggerated inflammation in ox-LDL-treated macrophages (10,11).…”

Section: Introductionmentioning

confidence: 99%

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Long Non-Coding RNAs Link Oxidized Low-Density Lipoprotein With the Inflammatory Response of Macrophages in Atherogenesis

Yan

Song

et al. 2020

Front. Immunol.

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Atherosclerosis is characterized as a chronic inflammatory response to cholesterol deposition in arteries. Low-density lipoprotein (LDL), especially the oxidized form (ox-LDL), plays a crucial role in the occurrence and development of atherosclerosis by inducing endothelial cell (EC) dysfunction, attracting monocyte-derived macrophages, and promoting chronic inflammation. However, the mechanisms linking cholesterol accumulation with inflammation in macrophage foam cells are poorly understood. Long non-coding RNAs (lncRNAs) are a group of non-protein-coding RNAs longer than 200 nucleotides and are found to regulate the progress of atherosclerosis. Recently, many lncRNAs interfering with cholesterol deposition or inflammation were identified, which might help elucidate their underlying molecular mechanism or be used as novel therapeutic targets. In this review, we summarize and highlight the role of lncRNAs linking cholesterol (mainly ox-LDL) accumulation with inflammation in macrophages during the process of atherosclerosis.

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Section: Macrophage Receptors Involved In Lipid Accumulation and Inflmentioning

confidence: 99%

Section: Lncrna Biology and Function In Atherosclerosismentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Long Non-Coding RNAs Link Oxidized Low-Density Lipoprotein With the Inflammatory Response of Macrophages in Atherogenesis

Yan

Song

et al. 2020

Front. Immunol.

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“…Long non-coding RNAs (lncRNAs) are non-protein coding transcripts that are composed of >200 nucleotides, and studies have demonstrated that certain lncRNAs have important functions in the regulation of numerous biological processes, including cell proliferation, differentiation and death (28)(29)(30). Metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is a widely expressed single-exon lncRNA.…”

Section: Introductionmentioning

confidence: 99%

Exosomal MALAT1 derived from oxidized low-density lipoprotein-treated endothelial cells promotes M2 macrophage polarization

Huang

Han

et al. 2018

Mol Med Report

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Oxidized low-density lipoprotein (oxLDL)-induced injury and apoptosis of endothelial cells are important initial events in numerous cardiovascular diseases. Following activation by oxLDL, monocytes adhere to endothelial cells, migrate into the subendothelial spaces and then undergo differentiation into macrophages, which subsequently induces the formation of atherosclerotic lesions. However, the mechanisms underlying the activation of macrophage differentiation by oxLDL-treated endothelial cells remain unclear. In the present study, it was demonstrated that exosomal metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) was increased in oxLDL-treated human umbilical vein endothelial cells. When co-cultured with monocytes, exosomes extracted from oxLDL-treated HUVECs were endocytosed. Furthermore, exosomes derived from oxLDL-treated endothelial cells were revealed to promote M2 macrophage polarization, as reverse transcription-quantitative polymerase chain reaction, western blotting and ELISA analyses demonstrated increases in the expression of M2 macrophage markers, including macrophage mannose receptor 1 (also termed CD206), arginase-1 and interleukin (IL)-10, and decreases in the expression of the M1 macrophage marker, IL-12. Furthermore, the suppression of MALAT1 expression in monocytes was demonstrated to reverse exosome-mediated M2 macrophage polarization. In conclusion, the results of the present study revealed a novel mechanism underlying the onset of atherogenesis associated with endothelial cells and macrophages: Exosomal MALAT1 derived from oxLDL-treated endothelial cells promoted M2 macrophage polarization. This result may provide a novel scientific basis for the understanding of atherosclerosis progression.

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“…Endothelial cells, vascular smooth muscle cells and macrophages are the primary cells leading to atherosclerotic lesion formation (Tabas et al, 2015). Previous studies have demonstrated that lncRNAs regulate the functions of endothelial cells, smooth muscle cells and macrophages, suggesting that lncRNAs are emerging important players in the progression of atherosclerosis (Jian et al, 2016;Zhou et al, 2016). However, the underlying mechanisms of lncRNAs in CIH aggravating atherosclerosis are poorly understood, and the study of lncRNAs in CIH aggravating atherosclerosis is scarce.…”

Section: Introductionmentioning

confidence: 99%

Potential Role of mRNAs and LncRNAs in Chronic Intermittent Hypoxia Exposure-Aggravated Atherosclerosis

Zhang

Jiao

et al. 2020

Front. Genet.

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Atherosclerosis is the pathological basis of cardiovascular disease. Obstructive sleep apnea (OSA) aggravates atherosclerosis, and chronic intermittent hypoxia (CIH) as a prominent feature of OSA plays an important role during the process of atherosclerosis. The mechanisms of CIH in the development of atherosclerosis remain unclear. In the current study, we used microarray to investigate differentially expressed mRNAs and long non-coding RNAs (lncRNAs) in aorta from five groups of ApoE −/− mice fed with a high-fat diet and exposed to various conditions: normoxia for 8 weeks, CIH for 8 weeks, normoxia for 12 weeks, CIH for 12 weeks, or CIH for 8 weeks followed by normoxia for 4 weeks. Selected transcripts were validated in aorta tissues and RT-qPCR analysis showed correlation with the microarray data. Gene Ontology analysis and pathway enrichment analysis were performed to explore the mRNA function. Bioinformatic analysis indicated that short-term CIH induced up-regulated mRNAs involved in inflammatory response. Pathway enrichment analysis of lncRNA colocalized mRNAs and lncRNA co-expressed mRNAs were performed to explore lncRNA functions. The up-regulated mRNAs, lncRNA co-localized mRNAs and lncRNA coexpressed mRNAs were significantly associated with protein processing in endoplasmic reticulum pathway in atherosclerotic vascular tissue with long-term CIH exposure, suggesting that differentially expressed mRNAs and lncRNAs play important roles in this pathway. Moreover, a mRNA-lncRNA co-expression network with 380 lncRNAs, 508 mRNAs and 3238 relationships was constructed based on the correlation analysis between the differentially expressed mRNAs and lncRNAs. In summary, our study provided a systematic perspective on the potential function of mRNAs and lncRNAs in CIH-aggravated atherosclerosis, and may provide novel molecular candidates for future investigation on atherosclerosis exposed to CIH.

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Long noncoding RNAs and atherosclerosis

Cited by 81 publications

References 124 publications

Long Non-Coding RNAs Link Oxidized Low-Density Lipoprotein With the Inflammatory Response of Macrophages in Atherogenesis

Long Non-Coding RNAs Link Oxidized Low-Density Lipoprotein With the Inflammatory Response of Macrophages in Atherogenesis

Exosomal MALAT1 derived from oxidized low-density lipoprotein-treated endothelial cells promotes M2 macrophage polarization

Potential Role of mRNAs and LncRNAs in Chronic Intermittent Hypoxia Exposure-Aggravated Atherosclerosis

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