Current issue
Archive
Manuscripts accepted
About the Journal
Editorial office
Editorial board
Abstracting and indexing
Subscription
Contact
Ethical standards and procedures
Most read articles
Instructions for authors
Article Processing Charge (APC)
Regulations of paying article processing charge (APC)
ATHEROSCLEROSIS / EXPERIMENTAL RESEARCH
Network analysis of the effects of long non-coding RNAs in artemisinin treatment of atherosclerosis in APOE–/– mice
1
Department of Cardiology, Shenjing Hospital of China Medical University, Shenyang, Liaoning, China
Submission date: 2019-08-09
Final revision date: 2020-02-08
Acceptance date: 2020-02-22
Online publication date: 2021-03-28
Corresponding author
Li Xiaodong
Department of Cardiology, Shenjing Hospital of China Medical University, Shenyang, Liaoning, China
Department of Cardiology, Shenjing Hospital of China Medical University, Shenyang, Liaoning, China
Arch Med Sci 2024;20(3):967-976
KEYWORDS
TOPICS
ABSTRACT
Introduction:
Atherosclerosis has become a worldwide medical burden. Our previous studies have shown that artemisinin (ART) had the capability to reduce atherosclerosis. Emerging evidence indicates that long non-coding RNAs (lncRNAs) are involved in the development of atherosclerosis. However, whether lncRNAs might participate in the mechanism through which artemisinin mitigates atherosclerosis has not been reported.
Material and methods:
Eight-week-old apolipoprotein E deficient (APOE–/–) mice were divided into two groups, one of which was treated with artemisinin. Red oil O staining was used to measure the sizes of the atherosclerotic lesions. We conducted deep sequencing to investigate lncRNA profiles in the aorta tissue in high-fat diet fed APOE knockdown mice with and without artemisinin treatment. CeRNA network, Kyoto Encyclopedia of Genes and Genomes (KEGG) and Gene Ontology (GO) analyses were performed through bioinformatics analysis. RT-PCR was used to validate the differentially expressed lncRNAs.
Results:
A total of 102 lncRNAs and 4,630 mRNAs were differentially expressed (p < 0.05) between the artemisinin treatment group and atherosclerosis model group. KEGG and GO analyses indicated that the categories metabolic process, specific amino acid degradation and PI3K-Akt signaling pathway are involved in the effects of artemisinin treatment in atherosclerosis (q < 0.05). LncRNA ENSMUST00000099676.4, ENSMUST00000143673.1, ENSMUST00000070085.5 and ENSMUST00000224554 might be engaged in the treatment mechanism through which artemisinin alleviates atherosclerosis.
Conclusions:
These findings indicated the possible mechanism and therapeutic role of lncRNAs in artemisinin treatment of atherosclerosis and provided a theoretical basis for the future application of artemisinin in patients with atherosclerosis.
Atherosclerosis has become a worldwide medical burden. Our previous studies have shown that artemisinin (ART) had the capability to reduce atherosclerosis. Emerging evidence indicates that long non-coding RNAs (lncRNAs) are involved in the development of atherosclerosis. However, whether lncRNAs might participate in the mechanism through which artemisinin mitigates atherosclerosis has not been reported.
Material and methods:
Eight-week-old apolipoprotein E deficient (APOE–/–) mice were divided into two groups, one of which was treated with artemisinin. Red oil O staining was used to measure the sizes of the atherosclerotic lesions. We conducted deep sequencing to investigate lncRNA profiles in the aorta tissue in high-fat diet fed APOE knockdown mice with and without artemisinin treatment. CeRNA network, Kyoto Encyclopedia of Genes and Genomes (KEGG) and Gene Ontology (GO) analyses were performed through bioinformatics analysis. RT-PCR was used to validate the differentially expressed lncRNAs.
Results:
A total of 102 lncRNAs and 4,630 mRNAs were differentially expressed (p < 0.05) between the artemisinin treatment group and atherosclerosis model group. KEGG and GO analyses indicated that the categories metabolic process, specific amino acid degradation and PI3K-Akt signaling pathway are involved in the effects of artemisinin treatment in atherosclerosis (q < 0.05). LncRNA ENSMUST00000099676.4, ENSMUST00000143673.1, ENSMUST00000070085.5 and ENSMUST00000224554 might be engaged in the treatment mechanism through which artemisinin alleviates atherosclerosis.
Conclusions:
These findings indicated the possible mechanism and therapeutic role of lncRNAs in artemisinin treatment of atherosclerosis and provided a theoretical basis for the future application of artemisinin in patients with atherosclerosis.
REFERENCES (32)
1.
O’Neill LAJ, Kishton RJ, Rathmell J. A guide to immunometabolism for immunologists. Nat Rev Immunol 2016; 16: 553-65.
2.
Tuñón J, Badimón L, Bochaton-Piallat M-L, et al. Identifying the anti-inflammatory response to lipid lowering therapy: a position paper from the working group on atherosclerosis and vascular biology of the European Society of Cardiology. Cardiovasc Res 2019; 115: 10-9.
4.
Ketelhuth DFJ, Lutgens E, Bäck M, et al. Immunometabolism and atherosclerosis: perspectives and clinical significance: a position paper from the Working Group on Atherosclerosis and Vascular Biology of the European Society of Cardiology. Cardiovasc Res 2019; 115: 1385-92.
5.
Eken MK, Ersoy GS, Kaygusuz EI, et al. Etanercept protects ovarian reserve against ischemia/reperfusion injury in a rat model. Arch Med Sci 2019; 15: 1104-12.
6.
Lu D, Peng F, Li J, et al. Urotensin II promotes secretion of LTB4 through 5-lipoxygenase via the UT-ROS-Akt pathway in RAW264.7 macrophages. Arch Med Sci 2019; 15: 1065-72.
7.
White NJ. Qinghaosu (artemisinin): the price of success. Science 2008; 320: 330-4.
8.
Kumari A, Karnatak M, Singh D, et al. Current scenario of artemisinin and its analogues for antimalarial activity. Eur J Med Chem 2019; 163: 804-29.
9.
Shi C, Li H, Yang Y, Hou L. Anti-inflammatory and immunoregulatory functions of artemisinin and its derivatives. Mediators Inflamm 2015; 2015: 435713.
10.
Jiang Y, Du H, Liu X, Fu X, Li X, Cao Q. Artemisinin alleviates atherosclerotic lesion by reducing macrophage inflammation via regulation of AMPK/NF-B/NLRP3 inflammasomes pathway. J Drug Target 2020; 28: 70-9.
11.
Cao Q, Jiang Y, Shi J, et al. Artemisinin inhibits the proliferation, migration, and inflammatory reaction induced by tumor necrosis factor- in vascular smooth muscle cells through nuclear factor kappa B pathway. J Surg Res 2015; 194: 667-78.
12.
Jedynak M, Siemiątkowski A, Milewski R, Mroczko B, Szmitkowski M. Diagnostic effectiveness of soluble triggering receptor expressed on myeloid cells-1 in sepsis, severe sepsis and septic shock. Arch Med Sci 2019; 15: 713-21.
13.
Marchese FP, Raimondi I, Huarte M. The multidimensional mechanisms of long noncoding RNA function. Genome Biol 2017; 18: 206.
14.
Liu Y, Zheng L, Wang Q, Hu Y-W. Emerging roles and mechanisms of long noncoding RNAs in atherosclerosis. Int J Cardiol 2017; 228: 570-82.
15.
Du H, Zhao Q, Zang H, Chang C, Li X. Artemisinin attenuates the development of atherosclerotic lesions by the regulation of vascular smooth muscle cell phenotype switching. Life Sci 2019; 237: 116943.
16.
Poredoš P, Spirkoska A, Ježovnik MK. In patients with superficial vein thrombosis the inflammatory response is increased and related to the recanalization rate. Arch Med Sci 2019; 15: 393-401.
17.
Cao L, Zhang Z, Li Y, Zhao P, Chen Y. LncRNA H19/miR-let-7 axis participates in the regulation of ox-LDL-induced endothelial cell injury via targeting periostin. Int Immunopharmacol 2019; 72: 496-503.
18.
Tian D, Sha Y, Lu J-M, Du X-J. MiR-370 inhibits vascular inflammation and oxidative stress triggered by oxidized low-density lipoprotein through targeting TLR4. J Cell Biochem 2018; 119: 6231-7.
19.
Kanno S, Nishio H, Tanaka T, et al. Activation of an innate immune receptor, Nod1, accelerates atherogenesis in Apoe −/− mice. J Immunol 2015; 194: 773-80.
20.
Bai L, Ni HM, Chen X, DiFrancesca D, Yin XM. Deletion of bid impedes cell proliferation and hepatic carcinogenesis. Am J Pathol 2005; 166: 1523-32.
21.
Warfel JM, D’Agnillo F. Anthrax lethal toxin enhances TNF-induced endothelial VCAM-1 expression via an IFN regulatory factor-1-dependent mechanism. J Immunol 2008; 180: 7516-24.
22.
Wu C, Xue Y, Wang P, et al. IFN- primes macrophage activation by increasing phosphatase and tensin homolog via downregulation of miR-3473b. J Immunol 2014; 193: 3036-44.
23.
Wang W, Zhang Y, Wang L, et al. MircroRNA-152 prevents the malignant progression of atherosclerosis via down-regulation of KLF5. Biomed Pharmacother 2019; 109: 2409-14.
24.
Zhang L, Cheng H, Yue Y, Li S, Zhang D, He R. H19 knockdown suppresses proliferation and induces apoptosis by regulating miR-148b/WNT/-catenin in ox-LDL -stimulated vascular smooth muscle cells. J Biomed Sci 2018; 25: 11.
25.
Boettger T, Beetz N, Kostin S, et al. Acquisition of the contractile phenotype by murine arterial smooth muscle cells depends on the Mir143/145 gene cluster. J Clin Invest 2009; 119: 2634-47.
26.
Bao M, Zhang Y, Lou X, Cheng Y, Zhou H. Protective effects of let-7a and let-7b on oxidized low-density lipoprotein induced endothelial cell injuries. PLoS One 2014; 9: e106540.
27.
Yang X, Zhang Q, Gao Z, Yu C, Zhang L. Down-regulation of MiR-150 alleviates inflammatory injury induced by interleukin 1 via targeting Kruppel-like factor 2 in human chondrogenic cells. Cell Physiol Biochem 2018; 47: 2579-88.
28.
Lan G, Xie W, Li L, et al. MicroRNA-134 actives lipoprotein lipase-mediated lipid accumulation and inflammatory response by targeting angiopoietin-like 4 in THP-1 macrophages. Biochem Biophys Res Commun 2016; 472: 410-7.
29.
Cheng HP, Gong D, Zhao ZW, et al. MicroRNA-182 promotes lipoprotein lipase expression and atherogenesisby targeting histone deacetylase 9 in apolipoprotein e-knockout mice. Circ J 2018; 82: 28-38.
30.
Kim YM, Stone M, Hwang TH, et al. SH3BP4 is a negative regulator of amino acid-Rag GTPase-mTORC1 signaling. Mol Cell 2012; 46: 833-46.
31.
Nozaki M, Raisler BJ, Sakurai E, et al. Drusen complement components C3a and C5a promote choroidal neovascularization. Proc Natl Acad Sci USA 2006; 103: 2328-33.
32.
Grajeda-Iglesias C, Aviram M. Specific amino acids affect cardiovascular diseases and atherogenesis via protection against macrophage foam cell formation: review article. Rambam Maimonides Med J 2018; 9: e0022.
Share
RELATED ARTICLE
| eISSN: | 1896-9151 |
| ISSN: | 1734-1922 |
We process personal data collected when visiting the website. The function of obtaining information about users and their behavior is carried out by voluntarily entered information in forms and saving cookies in end devices. Data, including cookies, are used to provide services, improve the user experience and to analyze the traffic in accordance with the Privacy policy. Data are also collected and processed by Google Analytics tool (more).
You can change cookies settings in your browser. Restricted use of cookies in the browser configuration may affect some functionalities of the website.
You can change cookies settings in your browser. Restricted use of cookies in the browser configuration may affect some functionalities of the website.
