scholarly journals LINC01534 promotes the aberrant metabolic dysfunction and inflammation in IL-1β-simulated osteoarthritic chondrocytes by targeting miR-140-5p

2019 ◽  
Author(s):  
Wei Wei ◽  
Shaoxuan He ◽  
Zhihua Wang ◽  
Junjie Dong ◽  
Dong Xiang ◽  
...  
Keyword(s):  
Inhibitory Effect ◽  
Cartilage Tissue ◽  
Inflammatory Factors ◽  
Metabolic Dysfunction ◽  
Matrix Degradation ◽  
Non Coding Rna ◽  
Osteoarthritic Chondrocytes ◽  
Tnf Α ◽  
Collagen Ii ◽  
Long Non Coding Rna

Abstract Backgrounds: Long non-coding RNA 01534 (LINC01534) is highly expressed in the tissues of patients with osteoarthritis (OA). This study investigated the mechanism of LINC01534 on abnormal metabolic dysfunction and inflammation in OA chondro-cytes induced by IL-1β. Methods: The quantitative Real-Time PCR (qRT-PCR) was used to determine the expressions of LINC01534, aggrecan, collagen II and matrix metalloproteinase (MMPs) in OA cartilage tissue or OA chondrocyte model induced by IL-1β. The ex-pressions of aggrecan and collagen II in the chondrocyte were detected by Western Blot. The levels of TNF-α, IL-8, IL-6, MMP-13, MMP-9, MMP-3 and prostaglandin E2 (PGE2) in chondrocyte were determined by ELISA. Bioinformatics, dual luciferin gene reporting, RNA pulldown and Northern Blot were used to determine the interac-tion between LINC01534 and miR-140-5p. Results: The results showed that LINC01534 was up-regulated in both OA cartilage tissue and OA chondrocyte model. In addition, silencing LINC01534 significantly alleviated the inhibitory effect of IL-1β on expressions of aggrecan and collagen II in chondrocytes, and significantly down-regulated the expression of matrix metallopro-teinases in IL-1β-induced chondrocytes. Meanwhile, silencing LINC01534 also sig-nificantly inhibited the productions of pro-inflammatory factors NO, PGE2, TNF-α, IL-6 and IL-8 in the IL-1β-induced chondrocytes. Furthermore, miR-140-5p was con-firmed to be a direct target of LINC01534. More importantly, inhibition of miR-140-5p significantly reversed the inhibitory effect of silencing LINC01534 on inflammation and abnormal matrix degradation in the IL-1β-induced chondrocyte model of OA. Conclusion: Therefor, LINC01534 could promote the abnormal matrix degradation and inflammatory response of OA chondrocytes through the targeted binding of miR-140-5p.

LINC01534 Promotes the Aberrant Metabolic Dysfunction and Inflammation in IL-1β-Simulated Osteoarthritic Chondrocytes by Targeting miR-140-5p

Cartilage ◽  
2019 ◽  
pp. 194760351988878 ◽  
Author(s):  
Wei wei ◽  
Shaoxuan He ◽  
Zhihua Wang ◽  
Junjie Dong ◽  
Dong Xiang ◽  
...  
Keyword(s):  
Inhibitory Effect ◽  
Cartilage Tissue ◽  
Metabolic Dysfunction ◽  
Matrix Degradation ◽  
Non Coding Rna ◽  
Osteoarthritic Chondrocytes ◽  
Tnf Α ◽  
Oa Chondrocytes ◽  
Collagen Ii ◽  
Factor Α

Objective Long non-coding RNA 01534 (LINC01534) is highly expressed in the tissues of patients with osteoarthritis (OA). This study investigated the mechanism of LINC01534 on abnormal metabolic dysfunction in OA chondrocytes induced by interleukin-1β (IL-1β). Methods The quantitative real-time polymerase chain reaction (qRT-PCR) was used to determine the expressions of LINC01534, aggrecan, collagen II, and matrix metalloproteinase (MMPs) in OA cartilage tissue or OA chondrocyte model induced by IL-1β. The expressions of aggrecan and collagen II in the chondrocyte were detected by Western blot. The levels of tumor necrosis factor–α (TNF-α), IL-8, IL-6, MMP-13, MMP-9, MMP-3, and prostaglandin E2 (PGE2) in chondrocyte were determined by enzyme-linked immunosorbernt assay. Bioinformatics, dual luciferin gene reporting, RNA pulldown, and Northern blot were used to determine the interaction between LINC01534 and miR-140-5p. Results The results showed that LINC01534 was upregulated in both OA cartilage tissue and OA chondrocyte model. In addition, silencing LINC01534 significantly alleviated the inhibitory effect of IL-1β on expressions of aggrecan and collagen II in chondrocytes, and significantly downregulated the expression of matrix metalloproteinases in IL-1β-induced chondrocytes. Meanwhile, silencing LINC01534 also significantly inhibited the productions of proinflammatory factors NO, PGE2, TNF-α, IL-6, and IL-8 in the IL-1β-induced chondrocytes. Furthermore, miR-140-5p was confirmed to be a direct target of LINC01534. More importantly, inhibition of miR-140-5p significantly reversed the inhibitory effect of silencing LINC01534 on abnormal matrix degradation in the IL-1β-induced chondrocyte model of OA. Conclusion Therefore, LINC01534 could promote the abnormal matrix degradation and inflammatory response of OA chondrocytes through the targeted binding of miR-140-5p.

scholarly journals LncRNA SNHG1 alleviates IL-1β-induced osteoarthritis by inhibiting miR-16-5p-mediated p38 MAPK and NF-κB signaling pathways

2019 ◽  
Vol 39 (9) ◽  
Author(s):  
Jinlai Lei ◽  
Yahui Fu ◽  
Yan Zhuang ◽  
Kun Zhang ◽  
Daigang Lu
Keyword(s):  
Signaling Pathways ◽  
Luciferase Reporter ◽  
Metabolic Dysfunction ◽  
Reporter Assay ◽  
Non Coding Rna ◽  
Tnf Α ◽  
Normal Human ◽  
Long Non Coding Rna ◽  
Nucleolar Rna ◽  
Pro Inflammatory Cytokines

Abstract Long non-coding RNA (LncRNA) small nucleolar RNA host gene 1 (SNHG1) has been reported in the occurrence and development of several diseases, but its biological role and mechanism in osteoarthritis (OA) remain to be illuminated. In the present research, we aimed to investigate the effect of SNHG1 on IL-1β-induced OA and its molecular mechanism. Results revealed that SNHG1 decreased the expression of MMPs, ADAMTs, collagen, and aggrecan, and ameliorates IL-1β-induced metabolic dysfunction in normal human chondrocytes-keen. In addition, SNHG1 inhibited the expressions of pro-inflammatory cytokines in chondrocytes, including NO, PGE2, IL-6, TNF-α, i-NOS, and COX-2. Furthermore, luciferase reporter assay demonstrated that SNHG1 could directly interact with miR-16-5p and suppressed miR-16-5p expression and activity. What is more, miR-16-5p overexpression reversed SNHG1-inhibited aberrant catabolism and inflammation triggered by IL-1β stimulation. Finally, SNHG1 inhibits the expression of miR-16-5p-mediated factors involved in p38MAPK and NF-κB signaling pathways, including ERK1/2, p-p38 and p-p65. Taken together, the results of our studies illuminate that SNHG1 alleviates the inflammation of IL-1β-induced OA through the activation of miR-16-5p-mediated p38MAPK and NF-κB signaling pathway. It suggested that SNHG1 may serve as a potential target for OA diagnosis and treatment.

scholarly journals Long Non-Coding RNA DANCR Participates in the Regulation of Dexamethasone and Inflammation Factors on hASC Proliferation and Migration

2021 ◽  
Author(s):  
Ran Yan ◽  
Ping Dong ◽  
Zhigang Yang ◽  
Rui Cao ◽  
Xia Liu ◽  
...  
Keyword(s):  
Cell Counting ◽  
Inflammatory Factors ◽  
Dependent Manner ◽  
Migration Ability ◽  
Non Coding Rna ◽  
Tnf Α ◽  
The Mean ◽  
And Migration ◽  
Long Non Coding Rna ◽  
Proliferation And Migration

Abstract BackgroundBoth MSC and Dexamethasone are effective methods to treat inflammatory diseases, and they are likely to be used in combination. The proliferation and migration ability is one of the main biological characteristics of MSC for repairing. However, the effect of inflammatory factors and Dex on these characteristics of MSC has not been fully understood. Therefore, this study aimed to determine the role of lncRNA DANCR in hASC proliferation and migration regulation induced by Dex and inflammatory factors, to clarify the effect and mechanism of glucocorticoids on MSC's characteristics to participate in tissue repair in an inflammatory environment. MethodshASCs were cultured and treated with dexamethasone and inflammation factors, and cell proliferation, migration abilities, and lncRNA DANCR mRNA expression were detected. Additionally, to determine the roles and mechanisms, lncRNA DANCR was knockdown or overexpressed before Dex or TNF-α treatments. MSC proliferation was tested by cell counting kit-8 and cell cycle assay. MSC migration ability was analyzed by a scratching test. Moreover, proliferation and migration-related genes were measured by a reverse transcription-polymerase chain reaction. Nuclear factor-kB (NF-κB) and PI3K-AKT-mTOR pathway proteins were investigated by western blot analysis. All values are expressed as the mean ± standard error of the mean. The differences between the groups were assessed using a two-tailed Student’s t-test. ResultsDex decreased the proliferation and migration of hASC in a dose-dependent manner. Dex could upregulate the expression of lncRNA DANCR that inhibited hASC proliferation and migration. Knockdown of DANCR reversed the inhibition of hASC proliferation and migration induced by Dex. Moreover, DANCR was decreased by inflammatory cytokines, and overexpression of DANCR alleviated the promotion of hASC proliferation and migration induced by TNF-α. Furthermore, mechanistic investigation validated that DANCR was involved in the NF-κB signaling pathway. ConclusionsWe identified a lncRNA, DANCR, involved in Dex and inflammation-affected hASC proliferation and migration, thus suggesting that concurrent application of hASCs with steroids should be avoided in clinical settings. DANCR may serve as a promising approach to regulate stem cell characteristics under an inflamed microenvironment. These findings further enrich our understanding of the functional versatility of lncRNAs in the crosstalk of inflammation conditions and stem cells. Keywords： DANCR; long non-coding RNA; Dexamethasone; TNF-α; hASC; proliferation; migration

scholarly journals Long non-coding RNA PVT1, a molecular sponge for miR-149, contributes aberrant metabolic dysfunction and inflammation in IL-1β-simulated osteoarthritic chondrocytes

2018 ◽  
Vol 38 (5) ◽  
Author(s):  
Yangxue Zhao ◽  
Jiang Zhao ◽  
Xufeng Guo ◽  
Jiang She ◽  
Yongjun Liu
Keyword(s):  
Inflammatory Response ◽  
Kidney Injury ◽  
Degenerative Joint Disease ◽  
Joint Disease ◽  
Mechanism Analysis ◽  
Metabolic Dysfunction ◽  
Non Coding Rna ◽  
Osteoarthritic Chondrocytes ◽  
Septic Acute Kidney Injury ◽  
Tnf Α

Osteoarthritis (OA), a common form of degenerative joint disease, is typified by inflammatory response and the loss of cartilage matrix. Long non-coding RNAs (lncRNAs) are emerging as a new player in gene regulation and exert critical roles in diverse physiologic and pathogenic processes including OA. The lncRNA plasmacytoma variant translocation 1 (PVT1) has been implicated in cancer, diabetes and septic acute kidney injury. Recent research confirmed the elevation of PVT1 in patients with OA. However, its role in the development of OA remains poorly elucidated. In the present study, high expression of PVT1 was observed in cartilage of OA patients and IL-1β-stimulated chondrocytes. Moreover, cessation of PVT1 expression dramatically reversed the inhibition of IL-1β on collagen II and aggrecan expression, but suppressed IL-1β-induced elevation of matrix metalloproteinases (MMPs), including MMP-3, MMP-9 and MMP-13. Simultaneously, PVT1 inhibition also antagonized the production of inflammatory cytokines upon IL-1β stimulation, including prostaglandin E2 (PGE2), NO, IL-6, IL-8 and TNF-α. Further molecular mechanism analysis identified PVT1 as an endogenous sponge RNA that could directly bind to miR-149 and repress its expression and activity. More importantly, miR-149 inhibition reversed the protective roles of PVT1 cessation in attenuating IL-1β-evoked matrix aberrant catabolism and inflammation. Together, this research confirms that lowering PVT1 expression may ameliorate the progression of OA by alleviating cartilage imbalance toward catabolism and inflammatory response, thus supporting a promising therapeutic strategy against OA.

scholarly journals The silencing of long non-coding RNA ANRIL suppresses invasion, and promotes apoptosis of retinoblastoma cells through the ATM-E2F1 signaling pathway

2018 ◽  
Vol 38 (6) ◽  
Author(s):  
Yang Yang ◽  
Xiao-Wei Peng
Keyword(s):  
Protein Expression ◽  
Signaling Pathway ◽  
Inhibitory Effect ◽  
Down Regulation ◽  
Reading Frame ◽  
Non Coding Rna ◽  
Retinoblastoma Cells ◽  
Human Retinoblastoma ◽  
Y79 Cells ◽  
Long Non Coding Rna

As one of the most common primary intraocular carcinomas, retinoblastoma generally stems from the inactivation of the retinoblastoma RB1 gene in retinal cells. Antisense non-coding RNA in the INK4 locus (ANRIL), a long non-coding RNA (lncRNA), has been reported to affect tumorigenesis and progression of various cancers, including gastric cancer and non-small cell lung cancer. However, limited investigations emphasized the role of ANRIL in human retinoblastoma. Hence, the current study was intended to investigate the effects of ANRIL on the proliferation, apoptosis, and invasion of retinoblastoma HXO-RB44 and Y79 cells. The lentivirus-based packaging system was designed to aid the up-regulation of ANRIL and ATM expressions or employed for the down-regulation of ANRIL in human retinoblastoma cells. Afterward, ANRIL expression, mRNA and protein expression of ATM and E2F1, and protein expression of INK4b, INK4a, alternate reading frame (ARF), p53 and retinoblastoma protein (pRB) were determined in order to elucidate the regulation effect associated with ANRIL on the ATM-E2F1 signaling pathway. In addition, cell viability, apoptosis, and invasion were detected accordingly. The results indicated that the down-regulation of ANRIL or up-regulation of ATM led to an increase in the expressions of ATM, E2F1, INK4b, INK4a, ARF, p53, and pRB. The silencing of ANRIL or up-regulation of ATM exerted an inhibitory effect on the proliferation and invasion while improving the apoptosis of HXO-RB44 and Y79 cells. In conclusion, the key observations of our study demonstrated that ANRIL depletion could act to suppress retinoblastoma progression by activating the ATM-E2F1 signaling pathway. These results provide a potentially promising basis for the targetted intervention treatment of human retinoblastoma.

scholarly journals Suppression of Long Non-Coding RNA LINC00652 Restores Sevoflurane-Induced Cardioprotection Against Myocardial Ischemia-Reperfusion Injury by Targeting GLP-1R Through the cAMP/PKA Pathway in Mice

2018 ◽  
Vol 49 (4) ◽  
pp. 1476-1491 ◽  
Author(s):  
Shu-Bo  Zhang ◽  
Tie-Jun Liu ◽  
Guo-Hua Pu ◽  
Bao-Yong Li ◽  
Xiao-Zeng Gao ◽  
...  
Keyword(s):  
Myocardial Ischemia ◽  
Cardiac Function ◽  
Infarct Size ◽  
Ischemia Reperfusion ◽  
Myocardial Cells ◽  
Non Coding Rna ◽  
Tnf Α ◽  
Myocardial Ischemia Reperfusion ◽  
Pka Pathway ◽  
Long Non Coding Rna

Background/Aims: Long non-coding RNA (lncRNA) and glucagon-like peptide 1 receptor (GLP-1R) are crucial for heart development and for adult heart structural maintenance and function. Herein, we performed a study to explore the effect of lncRNA LINC00652 (LINC00652) on myocardial ischemia-reperfusion (I/R) injury by targeting GLP-1R through the cyclic adenosine monophosphate-protein kinase A (cAMP/PKA) pathway. Methods: Bioinformatics software was used to screen the long-chain non-coding RNAs associated with myocardial ischemia-reperfusion and to predict target genes. The mRNA and protein levels of LINC00652, GLP-1R and CREB were detected by RT-qPCR and western blotting. In order to identify the interaction between LINC00652 and myocardial I/R injury, the cardiac function, the hemodynamic changes, the pathological changes of the myocardial tissues, the myocardial infarct size, and the apoptosis of myocardial cells of mice were measured. Meanwhile, the levels of serum IL-1β and TNF-α were detected. Results: LINC00652 was overexpressed in the myocardial cells of mice with myocardial I/R injury. GLP-1R is the target gene of LINC00652. We also determined higher levels of LINC00652 and GLP-1R in the I/R modeled mice. Additionally, si-LINC00652 decreased cardiac pathology, infarct size, apoptosis rates of myocardial cells, and levels of IL-1β and TNF-α, and increased GLP-1R expression cardiac function, normal hemodynamic index, and the expression and phosphorylation of GLP-1R and CREB proteins. Conclusion: Taken together, our key findings of the present highlight LINC00652 inhibits the activation of the cAMP/PKA pathway by targeting GLP-1R to reduce the protective effect of sevoflurane on myocardial I/R injury in mice.

scholarly journals Anti-Inflammatory Effects of Fucoxanthinol in LPS-Induced RAW264.7 Cells through the NAAA-PEA Pathway

Marine Drugs ◽  
2020 ◽  
Vol 18 (4) ◽  
pp. 222 ◽  
Author(s):  
Wenhui Jin ◽  
Longhe Yang ◽  
Zhiwei Yi ◽  
Hua Fang ◽  
Weizhu Chen ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Inhibitory Effect ◽  
Inflammatory Factors ◽  
Lipid Mediator ◽  
Peroxisome Proliferator ◽  
Necrosis Factor Alpha ◽  
Peroxisome Proliferator Activated Receptor ◽  
Tnf Α ◽  
Anti Inflammatory

Palmitoylethanolamide (PEA) is an endogenous lipid mediator with powerful anti-inflammatory and analgesic functions. PEA can be hydrolyzed by a lysosomal enzyme N-acylethanolamine acid amidase (NAAA), which is highly expressed in macrophages and other immune cells. The pharmacological inhibition of NAAA activity is a potential therapeutic strategy for inflammation-related diseases. Fucoxanthinol (FXOH) is a marine carotenoid from brown seaweeds with various beneficial effects. However, the anti-inflammatory effects and mechanism of action of FXOH in lipopolysaccharide (LPS)-stimulated macrophages remain unclear. This study aimed to explore the role of FXOH in the NAAA–PEA pathway and the anti-inflammatory effects based on this mechanism. In vitro results showed that FXOH can directly bind to the active site of NAAA protein and specifically inhibit the activity of NAAA enzyme. In an LPS-induced inflammatory model in macrophages, FXOH pretreatment significantly reversed the LPS-induced downregulation of PEA levels. FXOH also substantially attenuated the mRNA expression of inflammatory factors, including inducible nitric oxide synthase (iNOS), interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α), and markedly reduced the production of TNF-α, IL-6, IL-1β, and nitric oxide (NO). Moreover, the inhibitory effect of FXOH on NO induction was significantly abolished by the peroxisome proliferator-activated receptor α (PPAR-α) inhibitor GW6471. All these findings demonstrated that FXOH can prevent LPS-induced inflammation in macrophages, and its mechanisms may be associated with the regulation of the NAAA-PEA-PPAR-α pathway.

scholarly journals Inhibitory Effect of Metalloproteinase Inhibitors on Skin Cell Inflammation Induced by Jellyfish Nemopilema nomurai Nematocyst Venom

Toxins ◽  
2019 ◽  
Vol 11 (3) ◽  
pp. 156 ◽  
Author(s):  
Aoyu Li ◽  
Huahua Yu ◽  
Rongfeng Li ◽  
Song Liu ◽  
Ronge Xing ◽  
...  
Keyword(s):  
Inhibitory Effect ◽  
Research Area ◽  
Cellular Level ◽  
Inflammatory Factors ◽  
Nemopilema Nomurai ◽  
Whole Process ◽  
Skin Cell ◽  
Tnf Α ◽  
Main Components ◽  
Jellyfish Venom

Jellyfish envenomations result in extensive dermatological symptoms, clinically named as jellyfish dermatitis, which can seriously affect the daily activities and physical health of people. Inflammatory response accompanies the whole process of jellyfish dermatitis and the complexity of jellyfish venom components makes it difficult to treat jellyfish dermatitis symptoms effectively. Moreover, inhibiting inflammation is essential for the treatment of jellyfish stings and exploring the main components of jellyfish venom that cause inflammation is an urgent research area. In this study, the inhibitory effects of matrix metalloproteinase (MMP) inhibitors for venom-induced inflammation were explored at a cellular level. The expression of the three inflammatory factors, IL-6, TNF-α and MCP-1 in two skin cell lines, human keratinocyte cells (HaCaT) and human embryonic skin fibroblasts cells (CCC-ESF-1), at the cellular level, after treatment with the inhibitors of jellyfish Nemopilema nomurai (N. nomurai) nematocyst venom (NnNV-I), were determined. The results showed that inhibitors of MMP can significantly reduce the toxic effects of jellyfish Nemopilema nomurai nematocyst venom (NnNV) to skin cells. The expression levels of the three inflammatory factors IL-6, MCP-1, and TNF-α in the cells were also significantly decreased, indicating that MMPs in jellyfish venom are probably vital factors leading to jellyfish dermatitis. This study is beneficial in the prevention and treatment of jellyfish stings.

scholarly journals Correlation of Long Non-coding RNA LncRNA-FA2H-2 With Inflammatory Markers in the Peripheral Blood of Patients With Coronary Heart Disease

2021 ◽  
Vol 8 ◽  
Author(s):  
Fengxia Guo ◽  
Yanhua Sha ◽  
Bing Hu ◽  
Gang Li
Keyword(s):  
Cell Adhesion Molecule ◽  
Density Lipoprotein ◽  
Risk Groups ◽  
Gensini Score ◽  
Moderate Risk ◽  
Comparative Analyses ◽  
Non Coding Rna ◽  
Tnf Α ◽  
Cell Adhesion Molecule 1 ◽  
Long Non Coding Rna

Objective: To characterize the expression of long non-coding RNA LncRNA-FA2H-2 in coronary heart disease (CHD) and its correlation with inflammatory markers.Methods: From December 2018 to December 2020, 316 patients at Henan Provincial People's Hospital who complained of chest tightness or chest pain and had coronary angiography to clarify their coronary artery conditions for definitive diagnoses were selected as the study subjects. Plasma was collected to detect white blood cells (WBCs), total cholesterol (TG), triglyceride cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), apolipoprotein A1 (ApoA1), and C-reactive protein (CRP) levels. Tumor necrosis factor (TNF-α), monocyte chemotactic protein 1 (MCP-1), vascular cell adhesion molecule-1 (VCAM-1), intercellular cell adhesion molecule-1 (ICAM-1), and interleukin-6 (IL-6) levels were also measured using ELISA. The expression levels of lncRNA-FA2H-2 were measured using quantitative real-time PCR. The data obtained were analyzed by independent sample t-tests, rank sum tests, regression analyses, Pearson's or Spearman's correlation analyses, and receiver operating characteristic curves.Results: (1) Compared with the control group, the differences in age, sex, diabetes, smoking, drinking, body mass index (BMI), WBC, TC, and LDL-C in CHD were not statistically significant, while the differences in hypertension, TG, HDL-C, ApoA1, and CRP were statistically significant. (2) In the grouping of coronary lesion branches, patients with age, sex, hypertension, diabetes, smoking, drinking, BMI, WBC, TC, LDL-C, HDL-C, and ApoA1 differences were not statistically significant, but TG and CRP differences were statistically significant. (3) The relative expressions of TNF-α, MCP-1, VCAM-1, ICAM-1, and IL-6 were significantly upregulated in the CHD group (P < 0.001). (4) The results showed that the relative levels of TNF-α, MCP-1, VCAM-1, ICAM-1, and IL-6 between the two comparative analyses (high risk, moderate risk, and low risk groups) were statistically significant. In addition, positive correlations were found between the Gensini score and TNF-α, MCP-1, VCAM-1, ICAM-1, and IL-6 in CHD patients. (5) LncRNA-FA2H-2 relative expression in the CHD group was significantly downregulated (P < 0.001). (6) The differences in the expression levels of LncRNA-FA2H-2 were statistically significant between the two comparative analyses (P < 0.01), except between the 2-branch lesion and 3-branch lesion groups. (7) LncRNA-FA2H-2 was not associated with age, sex, hypertension, diabetes, smoking, drinking, BMI, WBC, TG, TC, LDL-C, HDL-C, and ApoA1 (P > 0.05). (8) A correlation was found between LncRNA-FA2H-2 and MCP-1, and VCAM-1, ICAM-1, IL-6, and Gensini. (9) The results indicated that the relative levels of LncRNA-FA2H-2 between the two comparative analyses (high risk, moderate risk, and low risk groups) were statistically significant. A negative correlation was found between the Gensini score and LncRNA-FA2H-2. (10) ROC curve analyses of TNF-α, MCP-1, VCAM-1, ICAM-1, and IL-6 in CHD showed the area under the curve (AUC) = 0.832 (0.77, 0.893) with a cut-off value of 290.5, a sensitivity of 73%, and a specificity of 64%; AUC = 0.731 (0.653, 0.809) with a cut-off value of 396 and with a sensitivity of 59% and specificity of 79%; AUC = 0.822 (0.757, 0.887) with a cut-off value of 264 and with a sensitivity of 72% and specificity of 83%; AUC = 0.794 (0.715, 0.874) with a cut-off value of 201.5 and with a sensitivity of 75% and specificity of 65%; AUC = 0.760 (0.685, 0.834) with a cut-off value of 328 and with a sensitivity of 55% and specificity of 90%. (11) ROC curve analysis of LncRNA-FA2H-2 in CHD patients showed AUC = 0.834 (0.688, 0.85) with a cut-off value of 3.155 and with a sensitivity of 85% and specificity of 82%. (12) Logistic analyses showed that TNF-α, MCP-1, VCAM-1, IL-6, and LncRNA-FA2H-2 were independent risk factors for CHD.Conclusions: The expression of LncRNA-FA2H-2 was reduced and inversely correlated with inflammation-related factors in CHD patients. LncRNA-FA2H-2 may have potential as an inflammatory marker for risk assessment of CHD development.

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