Circulating long noncoding <scp>RNA ANRIL</scp> downregulation correlates with increased risk, higher disease severity and elevated pro‐inflammatory cytokines in patients with acute ischemic stroke

Feng, Liqiang; Guo, Jun; Ai, Fen

doi:10.1002/jcla.22629

Cited by 54 publications

(37 citation statements)

References 21 publications

(40 reference statements)

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“…These studies suggest that lnc-ANRIL overexpression promotes inflammation, while lnc-anril knockdown reduces inflammation and alleviates neuronal injury. Notably, there are also studies illustrating an anti-inflammatory role of lnc-anril in various diseases (10,26). For example, a high expression of lnc-anril was associated with a decreased risk of acute exacerbation, pro-inflammatory cytokine expression and the global initiative for chronic obstructive lung disease stage in patients with chronic obstructive pulmonary disease (10).…”

Section: Discussionmentioning

confidence: 99%

Long non-coding RNA ANRIL knockdown suppresses apoptosis and pro-inflammatory cytokines while enhancing neurite outgrowth via binding microRNA-125a in a cellular model of Alzheimer's disease

Zhou

Qiu

et al. 2020

Mol Med Rep

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The present study aimed to investigate the effect of the long non-coding rna antisense non-coding rna in the inK4 locus (lnc-anril) knockdown on apoptosis, neurite outgrowth and inflammation based on a PC12 cellular alzheimer's disease (ad) model. a cellular ad model was constructed by treating nerve growth factor stimulated PC12 cells with amyloid β (aβ) 1-42 and then control knockdown plasmid and lnc-anril knockdown plasmid were transfected in the Pc12 cellular ad model as the Kd-negative control (nc) group or the ad-anril group respectively. Apoptosis, neurite outgrowth, pro-inflammatory cytokines and microrna (mir)-125a were assessed. rescue experiments were conducted by transfecting lnc-ANRIL knockdown plasmid and lnc-anril knockdown plasmid and mir-125a inhibitor in the PC12 cellular AD model as the KD-ANRIL group or Kd-anril + Kd-mir-125a group respectively. Following transfection, cell apoptosis deccreased while neurite outgrowth increased in the Kd-anril group compared with the Kd-nc group (all P<0.01). concerning inf lammation, tumor necrosis factor-α (TnF-α) and interleukin (il)-1β, il-6 and il-17 were decreased in the Kd-anril group compared with the Kd-nc group (all P<0.01). miR-125a was negatively regulated by lnc-ANRIL and therefore rescue experiments were subsequently conducted. in the rescue experiments, cell apoptosis was increased while total neurite outgrowth was inhibited in the Kd-anril + Kd-mir-125a group compared with the Kd-anril group (all P<0.01), and TnF-α, il-1β, il-6 and il-17 were increased in the Kd-anril + Kd-mir-125a group compared with the Kd-anril group (all P<0.01). a luciferase reporter assay demonstrated that lnc-ANRIL directly bound miR-125a. lnc-ANRIL knockdown suppressed cell apoptosis and inflammation while promoting neurite outgrowth via binding of miR-125a in AD.

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Section: Discussionmentioning

confidence: 99%

Long non-coding RNA ANRIL knockdown suppresses apoptosis and pro-inflammatory cytokines while enhancing neurite outgrowth via binding microRNA-125a in a cellular model of Alzheimer's disease

Zhou

Qiu

et al. 2020

Mol Med Rep

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“…Further study showed that ANRIL could enhance the viability of VSMCs via regulating miR-181a/silent information regulator 1 (SIRT1) (65). In addition, ANRIL downregulation correlated with elevated pro-inflammatory cytokines in patients with acute ischemic stroke, indicating ANRIL modulates inflammation (99). It was suggested that ANRIL could promote cholesterol efflux and inhibit inflammatory cytokines such as IL-1β and TNF-α in ox-LDL-exposed THP-1 macrophages by silencing ADAM (a disintegrin and metalloprotease) 10 (66).…”

Section: Anril (Cdkn2b-as1)mentioning

confidence: 98%

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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“…Numerous studies showed that lncRNAs are related to neuroinflammation and the activation of microglia in ischemic stroke. It was reported that the expression of lncRNA ANRIL was negatively associated with hs-CRP, TNF-α, and IL-6 levels, but positively correlated with IL-10 levels in AIS patients, suggesting that lncRNA ANRIL play an anti-inflammatory role in AIS progression (Feng et al, 2019). A recent study found that knockdown of lncRNA MALAT1 attenuated the inflammatory injury after brain ischemia, whereas overexpression of MALAT1 exacerbated ischemic brain inflammation (Cao et al, 2020).…”

Section: Lncrnas and Neuroinflammationmentioning

confidence: 99%

LncRNAs Stand as Potent Biomarkers and Therapeutic Targets for Stroke

Fan

Saft

Sadanandan

et al. 2020

Front. Aging Neurosci.

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Stroke is a major public health problem worldwide with a high burden of neurological disability and mortality. Long noncoding RNAs (lncRNAs) have attracted much attention in the past decades because of their newly discovered roles in pathophysiological processes in many diseases. The abundance of lncRNAs in the nervous system indicates that they may be part of a complex regulatory network governing physiology and pathology of the brain. In particular, lncRNAs have been shown to play pivotal roles in the pathogenesis of stroke. In this article, we provide a review of the multifaceted functions of lncRNAs in the pathogenesis of ischemic stroke and intracerebral hemorrhage, highlighting their promising use as stroke diagnostic biomarkers and therapeutics. To this end, we discuss the potential of stem cells in aiding lncRNA applications in stroke.

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Circulating long noncoding RNA ANRIL downregulation correlates with increased risk, higher disease severity and elevated pro‐inflammatory cytokines in patients with acute ischemic stroke

Abstract: Circulating lncRNA ANRIL downregulation correlates with increased stroke risk, higher disease severity and elevated inflammation in AIS patients.

Cited by 54 publications

References 21 publications

Long non-coding RNA ANRIL knockdown suppresses apoptosis and pro-inflammatory cytokines while enhancing neurite outgrowth via binding microRNA-125a in a cellular model of Alzheimer's disease

Long non-coding RNA ANRIL knockdown suppresses apoptosis and pro-inflammatory cytokines while enhancing neurite outgrowth via binding microRNA-125a in a cellular model of Alzheimer's disease

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

LncRNAs Stand as Potent Biomarkers and Therapeutic Targets for Stroke

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