کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8309121 | 1538502 | 2018 | 35 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
IL-13 enhances mesenchymal transition of pulmonary artery endothelial cells via down-regulation of miR-424/503 in vitro
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کلمات کلیدی
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
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چکیده انگلیسی
Pulmonary arterial hypertension (PAH) has a major effect on life expectancy with functional degeneracy of the lungs and right heart. Interleukin-13 (IL-13), one of the type 2 cytokines mainly associated with allergic diseases, has recently been reported to be associated with Schistosomiasis-associated PAH which shares pathological features with other forms of PAH, such as idiopathic PAH and connective tissue disease-associated PAH. But a direct pathological role of IL-13 in the development of PAH has not been explored. We examined the effects of recombinant human IL-13 on the function of primary human pulmonary artery endothelial cells (HPAECs) to examine how IL-13 influences exacerbation of PAH. IL-13 increased the expression of Rictor, which is a key molecule of mammalian target of rapamycin complex 2. Treatment of IL-13 induced HPAEC migration via Rictor. Rictor was directly regulated by both miR-424 and 503 (miR-424/503). Therefore, IL-13 increases Rictor level by regulating miR-424/503, causing the increase of HPAEC migration. Since enhancement of HPAEC migration in the lung is thought to be associated with PAH, these data suggest that IL-13 takes some roles in exacerbating PAH.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Cellular Signalling - Volume 42, January 2018, Pages 270-280
Journal: Cellular Signalling - Volume 42, January 2018, Pages 270-280
نویسندگان
Koichi Takagi, Munekazu Yamakuchi, Takahiro Matsuyama, Kiyotaka Kondo, Akifumi Uchida, Shunsuke Misono, Teruto Hashiguchi, Hiromasa Inoue,