Overexpression of microRNA-155 suppresses chemokine expression induced by Interleukin-13 in BEAS-2B human bronchial epithelial cells
Background: MicroRNAs are non-coding small RNAs that regulate expression of target genes by binding to 3′ untranslated regions. In this study, we used bronchial epithelial cells to investigate in vitro the role of the microRNA miR-155 in the expression of chemokines associated with airway inflammati...
| Main Authors: | , , , , , , , , , , , , , , , , , |
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| Format: | Article |
| Language: | English |
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Elsevier
2016-09-01
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| Series: | Allergology International |
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| Online Access: | http://www.sciencedirect.com/science/article/pii/S1323893016300594 |
| _version_ | 1819038240812826624 |
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| author | Satoshi Matsukura Yuki Osakabe Ayaka Sekiguchi Daisuke Inoue Yusuke Kakiuchi Toshitaka Funaki Yohei Yamazaki Hiromi Takayasu Hidetsugu Tateno Eisuke Kato Aya Wakabayashi Makoto Hayashi Gen Ishii Fumihiro Yamaguchi Yutaka Tsuchiya Keita Kasahara Hironori Sagara Fumio Kokubu |
| author_facet | Satoshi Matsukura Yuki Osakabe Ayaka Sekiguchi Daisuke Inoue Yusuke Kakiuchi Toshitaka Funaki Yohei Yamazaki Hiromi Takayasu Hidetsugu Tateno Eisuke Kato Aya Wakabayashi Makoto Hayashi Gen Ishii Fumihiro Yamaguchi Yutaka Tsuchiya Keita Kasahara Hironori Sagara Fumio Kokubu |
| author_sort | Satoshi Matsukura |
| collection | DOAJ |
| description | Background: MicroRNAs are non-coding small RNAs that regulate expression of target genes by binding to 3′ untranslated regions. In this study, we used bronchial epithelial cells to investigate in vitro the role of the microRNA miR-155 in the expression of chemokines associated with airway inflammation. miR-155 has previously been reported to regulate allergic inflammation.
Methods: BEAS-2B bronchial epithelial cells were cultured and transfected with mimic or inhibitor oligonucleotides to overexpress or downregulate miR-155, as confirmed by real-time PCR. Cells were then stimulated with tumor necrosis factor-alpha, interleukin-13 (IL-13), and a double stranded RNA that binds Toll-like receptor 3. Expression and secretion of the chemokines CCL5, CCL11, CCL26, CXCL8, and CXCL10 were then quantified by real-time PCR and ELISA, respectively. Phosphorylation of signal transducer and activator of transcription 6 (STAT6), a target of the IL-13 receptor, was analyzed by ELISA.
Results: miR-155 overexpression significantly suppressed IL-13-induced secretion of CCL11 and CCL26. These effects were specific, and were not observed for other chemokines, nor in cells with downregulated miR-155. miR-155 overexpression also suppressed CCL11 and CCL26 mRNA, but did not affect expression of the IL-13 receptor or phosphorylation of STAT6.
Conclusions: miR-155 specifically inhibits IL-13-induced expression of eosinophilic chemokines CCL11 and CCL26 in bronchial epithelial cells, even though the 3'-untranslated region of these genes do not contain a consensus binding site for miR-155. |
| first_indexed | 2024-12-21T08:34:10Z |
| format | Article |
| id | doaj.art-6b3c592b961b479ab6f70a1a0f55b62e |
| institution | Directory Open Access Journal |
| issn | 1323-8930 |
| language | English |
| last_indexed | 2024-12-21T08:34:10Z |
| publishDate | 2016-09-01 |
| publisher | Elsevier |
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| series | Allergology International |
| spelling | doaj.art-6b3c592b961b479ab6f70a1a0f55b62e2022-12-21T19:10:06ZengElsevierAllergology International1323-89302016-09-0165SS17S2310.1016/j.alit.2016.04.018Overexpression of microRNA-155 suppresses chemokine expression induced by Interleukin-13 in BEAS-2B human bronchial epithelial cellsSatoshi Matsukura0Yuki Osakabe1Ayaka Sekiguchi2Daisuke Inoue3Yusuke Kakiuchi4Toshitaka Funaki5Yohei Yamazaki6Hiromi Takayasu7Hidetsugu Tateno8Eisuke Kato9Aya Wakabayashi10Makoto Hayashi11Gen Ishii12Fumihiro Yamaguchi13Yutaka Tsuchiya14Keita Kasahara15Hironori Sagara16Fumio Kokubu17Department of Respiratory Internal Medicine, Showa University Fujigaoka Hospital, Kanagawa, JapanDepartment of Respiratory Internal Medicine, Showa University Fujigaoka Hospital, Kanagawa, JapanDepartment of Respiratory Internal Medicine, Showa University Fujigaoka Hospital, Kanagawa, JapanDepartment of Respiratory Internal Medicine, Showa University Fujigaoka Hospital, Kanagawa, JapanDepartment of Respiratory Internal Medicine, Showa University Fujigaoka Hospital, Kanagawa, JapanDepartment of Respiratory Internal Medicine, Showa University Fujigaoka Hospital, Kanagawa, JapanDepartment of Respiratory Internal Medicine, Showa University Fujigaoka Hospital, Kanagawa, JapanDepartment of Respiratory Internal Medicine, Showa University Fujigaoka Hospital, Kanagawa, JapanDepartment of Respiratory Internal Medicine, Showa University Fujigaoka Hospital, Kanagawa, JapanDepartment of Respiratory Internal Medicine, Showa University Fujigaoka Hospital, Kanagawa, JapanDepartment of Respiratory Internal Medicine, Showa University Fujigaoka Hospital, Kanagawa, JapanDepartment of Respiratory Internal Medicine, Showa University Fujigaoka Hospital, Kanagawa, JapanDepartment of Respiratory Internal Medicine, Showa University Fujigaoka Hospital, Kanagawa, JapanDepartment of Respiratory Internal Medicine, Showa University Fujigaoka Hospital, Kanagawa, JapanDepartment of Respiratory Internal Medicine, Showa University Fujigaoka Hospital, Kanagawa, JapanRespiratory Disease Center, Showa University Northern Yokohama Hospital, Kanagawa, JapanDepartment of Internal Medicine, Division of Allergy and Respiratory Medicine, Showa University School of Medicine, Tokyo, JapanDepartment of Respiratory Internal Medicine, Showa University Fujigaoka Hospital, Kanagawa, JapanBackground: MicroRNAs are non-coding small RNAs that regulate expression of target genes by binding to 3′ untranslated regions. In this study, we used bronchial epithelial cells to investigate in vitro the role of the microRNA miR-155 in the expression of chemokines associated with airway inflammation. miR-155 has previously been reported to regulate allergic inflammation. Methods: BEAS-2B bronchial epithelial cells were cultured and transfected with mimic or inhibitor oligonucleotides to overexpress or downregulate miR-155, as confirmed by real-time PCR. Cells were then stimulated with tumor necrosis factor-alpha, interleukin-13 (IL-13), and a double stranded RNA that binds Toll-like receptor 3. Expression and secretion of the chemokines CCL5, CCL11, CCL26, CXCL8, and CXCL10 were then quantified by real-time PCR and ELISA, respectively. Phosphorylation of signal transducer and activator of transcription 6 (STAT6), a target of the IL-13 receptor, was analyzed by ELISA. Results: miR-155 overexpression significantly suppressed IL-13-induced secretion of CCL11 and CCL26. These effects were specific, and were not observed for other chemokines, nor in cells with downregulated miR-155. miR-155 overexpression also suppressed CCL11 and CCL26 mRNA, but did not affect expression of the IL-13 receptor or phosphorylation of STAT6. Conclusions: miR-155 specifically inhibits IL-13-induced expression of eosinophilic chemokines CCL11 and CCL26 in bronchial epithelial cells, even though the 3'-untranslated region of these genes do not contain a consensus binding site for miR-155.http://www.sciencedirect.com/science/article/pii/S1323893016300594AsthmaBronchial epithelial cellsCCL11CCL26miR-155 |
| spellingShingle | Satoshi Matsukura Yuki Osakabe Ayaka Sekiguchi Daisuke Inoue Yusuke Kakiuchi Toshitaka Funaki Yohei Yamazaki Hiromi Takayasu Hidetsugu Tateno Eisuke Kato Aya Wakabayashi Makoto Hayashi Gen Ishii Fumihiro Yamaguchi Yutaka Tsuchiya Keita Kasahara Hironori Sagara Fumio Kokubu Overexpression of microRNA-155 suppresses chemokine expression induced by Interleukin-13 in BEAS-2B human bronchial epithelial cells Allergology International Asthma Bronchial epithelial cells CCL11 CCL26 miR-155 |
| title | Overexpression of microRNA-155 suppresses chemokine expression induced by Interleukin-13 in BEAS-2B human bronchial epithelial cells |
| title_full | Overexpression of microRNA-155 suppresses chemokine expression induced by Interleukin-13 in BEAS-2B human bronchial epithelial cells |
| title_fullStr | Overexpression of microRNA-155 suppresses chemokine expression induced by Interleukin-13 in BEAS-2B human bronchial epithelial cells |
| title_full_unstemmed | Overexpression of microRNA-155 suppresses chemokine expression induced by Interleukin-13 in BEAS-2B human bronchial epithelial cells |
| title_short | Overexpression of microRNA-155 suppresses chemokine expression induced by Interleukin-13 in BEAS-2B human bronchial epithelial cells |
| title_sort | overexpression of microrna 155 suppresses chemokine expression induced by interleukin 13 in beas 2b human bronchial epithelial cells |
| topic | Asthma Bronchial epithelial cells CCL11 CCL26 miR-155 |
| url | http://www.sciencedirect.com/science/article/pii/S1323893016300594 |
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