MicroRNAs as Potential Mediators for Cigarette Smoking Induced Atherosclerosis
| Autor: | Lingyi Zhang, Kiyora Izuoka, Yoshiji Yamada, Yuka Suzuki, Yuka Yokoyama, Cai Zong, Nathan Mise, Akira Takai, Sahoko Ichihara, Saeko Tada-Oikawa |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2018 |
| Předmět: |
0301 basic medicine
Apolipoprotein E lcsh:Chemistry Pathogenesis Mice Myocardial infarction lcsh:QH301-705.5 Aorta Chemokine CCL2 Spectroscopy NADPH oxidase biology cigarette smoke General Medicine Intercellular Adhesion Molecule-1 microRNAs Computer Science Applications NADPH Oxidase 2 medicine.symptom medicine.medical_specialty Vascular Cell Adhesion Molecule-1 Inflammation Article Catalysis Cigarette Smoking Inorganic Chemistry 03 medical and health sciences Apolipoproteins E Downregulation and upregulation Internal medicine medicine.artery medicine Animals Physical and Theoretical Chemistry Molecular Biology business.industry Organic Chemistry NADPH Oxidases Atherosclerosis Cytochrome b Group medicine.disease atherosclerosis 030104 developmental biology Endocrinology lcsh:Biology (General) lcsh:QD1-999 biology.protein P22phox business |
| Zdroj: | International Journal of Molecular Sciences; Volume 19; Issue 4; Pages: 1097 International Journal of Molecular Sciences International Journal of Molecular Sciences, Vol 19, Iss 4, p 1097 (2018) |
| ISSN: | 1422-0067 |
| DOI: | 10.3390/ijms19041097 |
| Popis: | Smoking increases the risk of atherosclerosis-related events, such as myocardial infarction and ischemic stroke. Recent studies have examined the expression levels of altered microRNAs (miRNAs) in various diseases. The profiles of tissue miRNAs can be potentially used in diagnosis or prognosis. However, there are limited studies on miRNAs following exposure to cigarette smoke (CS). The present study was designed to dissect the effects and cellular/molecular mechanisms of CS-induced atherosclerogenesis. Apolipoprotein E knockout (ApoE KO) mice were exposed to CS for five days a week for two months at low (two puffs/min for 40 min/day) or high dose (two puffs/min for 120 min/day). We measured the area of atherosclerotic plaques in the aorta, representing the expression of miRNAs after the exposure period. Two-month exposure to the high dose of CS significantly increased the plaque area in aortic arch, and significantly upregulated the expression of atherosclerotic markers (VCAM-1, ICAM-1, MCP1, p22phox, and gp91phox). Exposure to the high dose of CS also significantly upregulated the miRNA-155 level in the aortic tissues of ApoE KO mice. Moreover, the expression level of miR-126 tended to be downregulated and that of miR-21 tended to be upregulated in ApoE KO mice exposed to the high dose of CS, albeit statistically insignificant. The results suggest that CS induces atherosclerosis through increased vascular inflammation and NADPH oxidase expression and also emphasize the importance of miRNAs in the pathogenesis of CS-induced atherosclerosis. Our findings provide evidence for miRNAs as potential mediators of inflammation and atherosclerosis induced by CS. |
| Databáze: | OpenAIRE |
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