Silencing lncRNA AK136714 reduces endothelial cell damage and inhibits atherosclerosis

Bai, Jing; Liu, Jianxia; Fu, Zexian; Feng, Yuanyuan; Wang, Bing; Wu, Wenjuan; Zhang, Ruiying

doi:10.18632/aging.203031

Cited by 16 publications

(5 citation statements)

References 25 publications

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“…With the in-depth study of lncRNA, it is found that lncRNA is involved in the occurrence and development of AS [ 17 ]. Bai and colleagues certify that silenced lncRNA AK136714 inhibits atherosclerosis by down-regulating inflammatory responses and promoting apoptosis of HUVECs [ 18 ]. As a common lncRNA, the values of GASL1 are researched in several vascular disorders.…”

Section: Discussionmentioning

confidence: 99%

Upgulation of lncRNA GASL1 inhibits atherosclerosis by regulating miR-106a/LKB1 axis

Rui¹,

Rong³

et al. 2023

BMC Cardiovasc Disord

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Background Atherosclerosis (AS) is a common frequently-occurring disease in the clinic and a serious threat to human health. This research aimed to explore the value between GASL1 and AS. Methods The expression and values of GASL1 in AS patients were revealed by qRT-PCR and ROC curve. The HUVEC cells were induced by ox-LDL to construct in-vitro models. Cell viability was detected by MTT assay, and apoptosis was detected by flow cytometry. The inflammatory situation was reflected by the ELISA assay. Double luciferase reporter gene assay verified the regulatory relationship between GASL1 and miR-106a, miR-106a and LKB1. Results The levels of GASL1 was lower in AS group than those in control group. The value of GASL1 in predicting AS patients was also tested by the ROC curve. After HUVEC cells were induced by ox-LDL, the levels of GASL1 and LKB1 decreased significantly, while the level of miR-106a increased significantly. Upregulation of LKB1 reversed the effect of upregulation of GASL1 on viability, apoptosis, and inflammation of HUVEC cells induced by ox-LDL. Conclusion Overexpression of GASL1 might suppress ox-LDL-induced HUVEC cell viability, apoptosis, and inflammation by regulating miR-106a/LKB1 axis.

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Section: Discussionmentioning

confidence: 99%

Upgulation of lncRNA GASL1 inhibits atherosclerosis by regulating miR-106a/LKB1 axis

Rui¹,

Rong³

et al. 2023

BMC Cardiovasc Disord

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“…The lncRNA AK136714 was elevated in the plaque and plasma of the atherosclerosis patients. AK136714 knockdown could decrease IL-1β, IL-6, and TNF-α levels by binding directly to HuR to maintain mRNA stability, thereby protecting the endothelial barrier [ 24 ].…”

Section: Roles Of Lncrnas In Cardiovascular Diseasementioning

confidence: 99%

Roles of long noncoding RNAs in human inflammatory diseases

Zhang,

Liu,

Niu

et al. 2024

Cell Death Discov.

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Chemokines, cytokines, and inflammatory cells mediate the onset and progression of many diseases through the induction of an inflammatory response. LncRNAs have emerged as important regulators of gene expression and signaling pathways. Increasing evidence suggests that lncRNAs are key players in the inflammatory response, making it a potential therapeutic target for various diseases. From the perspective of lncRNAs and inflammatory factors, we summarized the expression level and regulatory mechanisms of lncRNAs in human inflammatory diseases, such as cardiovascular disease, osteoarthritis, sepsis, chronic obstructive pulmonary disease, asthma, acute lung injury, diabetic retinopathy, and Parkinson’s disease. We also summarized the functions of lncRNAs in the macrophages polarization and discussed the potential applications of lncRNAs in human inflammatory diseases. Although our understanding of lncRNAs is still in its infancy, these data will provide a theoretical basis for the clinical application of lncRNAs.

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“…AK136714 binds to HuR, also known as ELAVL1. HuR is a widely expressed RNA-binding protein that increases the stability of TNF-α, IL-1β and IL-6 mRNA, which promotes inflammation [55]. In addition, Ming-Peng and colleagues indicated the potential significance of the COLCA1 (colorectal cancer associated 1)/miR-371a-5p/SPP1 axis in atherosclerosis-related inflammation [56].…”

Section: Inflammatory Responsementioning

confidence: 99%

LncRNAs as Regulators of Atherosclerotic Plaque Stability

Petković

Erceg

Munjas

et al. 2023

Cells

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Current clinical data show that, despite constant efforts to develop novel therapies and clinical approaches, atherosclerotic cardiovascular diseases (ASCVD) are still one of the leading causes of death worldwide. Advanced and unstable atherosclerotic plaques most often trigger acute coronary events that can lead to fatal outcomes. However, despite the fact that different plaque phenotypes may require different treatments, current approaches to prognosis, diagnosis, and classification of acute coronary syndrome do not consider the diversity of plaque phenotypes. Long non-coding RNAs (lncRNAs) represent an important class of molecules that are implicated in epigenetic control of numerous cellular processes. Here we review the latest knowledge about lncRNAs’ influence on plaque development and stability through regulation of immune response, lipid metabolism, extracellular matrix remodelling, endothelial cell function, and vascular smooth muscle function, with special emphasis on pro-atherogenic and anti-atherogenic lncRNA functions. In addition, we present current challenges in the research of lncRNAs’ role in atherosclerosis and translation of the findings from animal models to humans. Finally, we present the directions for future lncRNA-oriented research, which may ultimately result in patient-oriented therapeutic strategies for ASCVD.

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Silencing lncRNA AK136714 reduces endothelial cell damage and inhibits atherosclerosis

Cited by 16 publications

References 25 publications

Upgulation of lncRNA GASL1 inhibits atherosclerosis by regulating miR-106a/LKB1 axis

Upgulation of lncRNA GASL1 inhibits atherosclerosis by regulating miR-106a/LKB1 axis

Roles of long noncoding RNAs in human inflammatory diseases

LncRNAs as Regulators of Atherosclerotic Plaque Stability

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