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  1. 学内発行誌
  2. 薬学部
  3. 薬学部研究年報
  4. 30

培養肺胞上皮細胞RLE-6TNにおけるインスリン取り込み機構(発表論文抄録(2011))

https://fukuyama-u.repo.nii.ac.jp/records/8825
https://fukuyama-u.repo.nii.ac.jp/records/8825
7ad3ed29-d307-4855-96d4-6d71366085f5
名前 / ファイル ライセンス アクション
30-23.pdf 小田啓祐(発表論文抄録(2011)) (104.7 kB)
Item type 紀要論文 / Departmental Bulletin Paper(1)
公開日 2017-12-25
タイトル
タイトル 培養肺胞上皮細胞RLE-6TNにおけるインスリン取り込み機構(発表論文抄録(2011))
タイトル
タイトル Mechanism underlying insulin uptake in alveolar epithelial cell line RLE-6TN.
言語 en
言語
言語 eng
キーワード
言語 en
主題Scheme Other
主題 Animals
キーワード
言語 en
主題Scheme Other
主題 Cell Line
キーワード
言語 en
主題Scheme Other
主題 Cell Polarity
キーワード
言語 en
主題Scheme Other
主題 Endocytosis
キーワード
言語 en
主題Scheme Other
主題 Epithelial Cells
キーワード
言語 en
主題Scheme Other
主題 Fluorescein-5-isothiocyanate
キーワード
言語 en
主題Scheme Other
主題 Gene Knockdown Techniques
キーワード
言語 en
主題Scheme Other
主題 Insulin
キーワード
言語 en
主題Scheme Other
主題 Intracellular Space
キーワード
言語 en
主題Scheme Other
主題 Protein Transport
キーワード
言語 en
主題Scheme Other
主題 Proteolysis
キーワード
言語 en
主題Scheme Other
主題 Pulmonary Alveoli
キーワード
言語 en
主題Scheme Other
主題 RNA, Small Interfering
キーワード
言語 en
主題Scheme Other
主題 Rats
キーワード
言語 en
主題Scheme Other
主題 Receptor, Insulin
資源タイプ
資源タイプ識別子 http://purl.org/coar/resource_type/c_6501
資源タイプ departmental bulletin paper
著者 Oda, Keisuke

× Oda, Keisuke

WEKO 46190

Oda, Keisuke

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Yumoto, Ryoko

× Yumoto, Ryoko

WEKO 46191

Yumoto, Ryoko

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Nagai, Junya

× Nagai, Junya

WEKO 46192

Nagai, Junya

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Katayama, Hirokazu

× Katayama, Hirokazu

WEKO 46193

Katayama, Hirokazu

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Takano, Mikihisa

× Takano, Mikihisa

WEKO 46194

Takano, Mikihisa

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著者別名
識別子Scheme WEKO
識別子 45890
識別子Scheme CiNii ID
識別子URI http://ci.nii.ac.jp/nrid/9000283797503
識別子 9000283797503
姓名 小田, 啓祐
著者別名
識別子Scheme WEKO
識別子 45891
識別子Scheme CiNii ID
識別子URI http://ci.nii.ac.jp/nrid/9000002748331
識別子 9000002748331
姓名 湯元, 良子
著者別名
識別子Scheme WEKO
識別子 45892
識別子Scheme CiNii ID
識別子URI http://ci.nii.ac.jp/nrid/9000003074469
識別子 9000003074469
姓名 永井, 純也
著者別名
識別子Scheme WEKO
識別子 45893
識別子Scheme CiNii ID
識別子URI http://ci.nii.ac.jp/nrid/9000002867742
識別子 9000002867742
姓名 片山, 博和
著者別名
識別子Scheme WEKO
識別子 45894
識別子Scheme CiNii ID
識別子URI http://ci.nii.ac.jp/nrid/9000002748332
識別子 9000002748332
姓名 高野, 幹久
抄録
内容記述タイプ Abstract
内容記述 For the development of efficient pulmonary delivery systems for protein and peptide drugs, it is important to understand their transport mechanisms in alveolar epithelial cells. In this study, the uptake mechanism for FITC-insulin in cultured alveolar epithelial cell line RLE-6TN was elucidated. FITC-insulin uptake by RLE-6TN cells was time-dependent, temperature-sensitive, and concentration-dependent. The uptake was inhibited by metabolic inhibitors, cytochalasin D, clathrin-mediated endocytosis inhibitors, and dynasore, an inhibitor of dynamin GTPase. On the other hand, no inhibitory effect was observed with caveolae-mediated endocytosis inhibitors and a macropinocytosis inhibitor. Intracellular FITC-insulin was found to be partly transported to the basal side of the epithelial cell monolayers. In addition, colocalization of FITC-insulin and LysoTracker Red was observed on confocal laser scanning microscopy, indicating that FITC-insulin was partly targeted to lysosomes. In accordance with these findings, SDS-PAGE/fluoroimage analysis showed that intact FITC-insulin in the cells was eliminated with time. The possible receptor involved in FITC-insulin uptake by RLE-6TN cells was examined by using siRNA. Transfection of the cells with megalin or insulin receptor siRNA successfully reduced the corresponding mRNA expression. FITC-insulin uptake decreased on the transfection with insulin receptor siRNA, but not that with megalin siRNA. These results suggest that insulin is taken up through endocytosis in RLE-6TN cells, and after the endocytosis, the intracellular insulin is partly degraded in lysosomes and partly transported to the basal side. Insulin receptor, but not megalin, may be involved at least partly in insulin endocytosis in RLE-6TN cells.
内容記述
内容記述タイプ Other
内容記述 For the development of efficient pulmonary delivery systems for protein and peptide drugs, it is important to understand their transport mechanisms in alveolar epithelial cells. In this study, the uptake mechanism for FITC-insulin in cultured alveolar epithelial cell line RLE-6TN was elucidated. FITC-insulin uptake by RLE-6TN cells was time-dependent, temperature-sensitive, and concentration-dependent. The uptake was inhibited by metabolic inhibitors, cytochalasin D, clathrin-mediated endocytosis inhibitors, and dynasore, an inhibitor of dynamin GTPase. On the other hand, no inhibitory effect was observed with caveolae-mediated endocytosis inhibitors and a macropinocytosis inhibitor. Intracellular FITC-insulin was found to be partly transported to the basal side of the epithelial cell monolayers. In addition, colocalization of FITC-insulin and LysoTracker Red was observed on confocal laser scanning microscopy, indicating that FITC-insulin was partly targeted to lysosomes. In accordance with these findings, SDS-PAGE/fluoroimage analysis showed that intact FITC-insulin in the cells was eliminated with time. The possible receptor involved in FITC-insulin uptake by RLE-6TN cells was examined by using siRNA. Transfection of the cells with megalin or insulin receptor siRNA successfully reduced the corresponding mRNA expression. FITC-insulin uptake decreased on the transfection with insulin receptor siRNA, but not that with megalin siRNA. These results suggest that insulin is taken up through endocytosis in RLE-6TN cells, and after the endocytosis, the intracellular insulin is partly degraded in lysosomes and partly transported to the basal side. Insulin receptor, but not megalin, may be involved at least partly in insulin endocytosis in RLE-6TN cells.
書誌情報 福山大学薬学部研究年報
en : Annual report of the Faculty of Pharmacy & Pharmaceutical Sciences, Fukuyama University

号 30, p. 23-24, 発行日 2012-12-25
出版者
出版者 福山大学薬学部
ISSN
収録物識別子タイプ ISSN
収録物識別子 0288-724X
書誌レコードID
収録物識別子タイプ NCID
収録物識別子 AN10064550
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