著者・編者Uchiyama, Tomoko
Itaya-Hironaka, Asako
Yamauchi, Akiyo
Makino, Mai
Sakuramoto-Tsuchida, Sumiyo
Shobatake, Ryogo
Ota, Hiroyo
Takeda, Maiko
Ohbayashi, Chiho
Takasawa, Shin
並列タイトル等間欺的低酸素被曝は、脂肪細胞においてmicro RNA-452の発現低下を介してCCL2、Resistin、TNFαの発現上昇を引き起こす
タイトル(掲載誌)International journal of molecular sciences
一般注記type:Thesis
Sleep apnea syndrome (SAS), characterized by recurrent episodes of oxygen desaturation and reoxygenation (intermittent hypoxia [IH]), is a risk factor for insulin resistance. Recently, IH is considered to independently cause adipose tissue inflammation/dysfunction, leading to worsening insulin resistance; however, the detailed mechanism remains unknown. We exposed mouse 3T3-L1 and human SW872 adipocytes to experimental IH or normoxia for 24 h, and analyzed mRNA expression of several adipokines. We found that the mRNA levels of RETN, TNFα, and CCL2 in SW872 and 3T3-L1 adipocytes were significantly increased by IH, whereas the promoter activities of these genes were not increased. A target mRNA search of microRNA (miR)s revealed that all human mRNAs have a potential target sequence for miR-452. The miR-452 level of IH-treated cells was significantly decreased compared to normoxia-treated cells. MiR-452 mimic and non-specific control RNA (miR-452 mimic NC) were introduced into SW872 cells, and the IH-induced up-regulation of the genes was abolished by introduction of the miR-452 mimic but not by the miR-452 mimic NC. These results indicate that IH stress down-regulates the miR-452 in adipocytes, resulting in increased levels of RETN, TNFα, and CCL2 mRNAs, leading to insulin resistance in SAS patients.
博士(医学)・甲第729号・令和2年3月16日
© 2019 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open accessarticle distributed under the terms and conditions of the Creative Commons Attribution(CC BY) license (http://creativecommons.org/licenses/by/4.0/).
identifier:International journal of molecular sciences Vol.20 No.8 Article No.1960 (2019 Apr)
identifier:14220067
identifier:http://ginmu.naramed-u.ac.jp/dspace/handle/10564/3720
identifier:International journal of molecular sciences, 20(8): Article No.1960
DOIinfo:doi/10.3390/ijms20081960
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