MicroRNAs as Potential Mediators for Cigarette Smoking Induced Atherosclerosis
by
Yuka Yokoyama 1, Nathan Mise 2
, Yuka Suzuki 3, Saeko Tada-Oikawa 3, Kiyora Izuoka 3, Lingyi Zhang 4, Cai Zong 4, Akira Takai 5, Yoshiji Yamada 1 and Sahoko Ichihara 1,2,3,*
Yuka Yokoyama 1, Nathan Mise 2, Yuka Suzuki 3, Saeko Tada-Oikawa 3, Kiyora Izuoka 3, Lingyi Zhang 4, Cai Zong 4, Akira Takai 5, Yoshiji Yamada 1 and Sahoko Ichihara 1,2,3,*
1
Department of Human Functional Genomics, Advanced Science Research Promotion Center, Mie University, 1577 Kurimamachiya, Tsu 514-8507, Japan
2
Department of Environmental and Preventive Medicine, School of Medicine, Jichi Medical University, 3311-1, Yakushiji, Shimotsuke 329-0498, Japan
3
Graduate School of Regional Innovation Studies, Mie University, 1577 Kurimamachiya, Tsu 514-8507, Japan
4
Department of Occupational and Environmental Health, Tokyo University of Science, 2641 Yamazaki, Noda 278-8510, Japan
5
Department of Physiology, Asahikawa Medical College, 2-1-1-1 Midorigaoka Higashi, Asahikawa 078-8510, Japan
*
Author to whom correspondence should be addressed.
Int. J. Mol. Sci. 2018, 19(4), 1097; https://doi.org/10.3390/ijms19041097
Received: 27 February 2018 / Revised: 2 April 2018 / Accepted: 2 April 2018 / Published: 6 April 2018
(This article belongs to the Special Issue The Role of MicroRNAs in Human Diseases)
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.
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Keywords:
cigarette smoke; atherosclerosis; NADPH oxidase; microRNAs
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MDPI and ACS Style
Yokoyama, Y.; Mise, N.; Suzuki, Y.; Tada-Oikawa, S.; Izuoka, K.; Zhang, L.; Zong, C.; Takai, A.; Yamada, Y.; Ichihara, S. MicroRNAs as Potential Mediators for Cigarette Smoking Induced Atherosclerosis. Int. J. Mol. Sci. 2018, 19, 1097.
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