ログイン
言語:

WEKO3

  • トップ
  • ランキング
To
lat lon distance
To

Field does not validate



インデックスリンク

インデックスツリー

メールアドレスを入力してください。

WEKO

One fine body…

WEKO

One fine body…

アイテム

{"_buckets": {"deposit": "ceb25fe6-3b46-4e5b-863e-000afaeb043c"}, "_deposit": {"id": "2016141", "owners": [1], "pid": {"revision_id": 0, "type": "depid", "value": "2016141"}, "status": "published"}, "_oai": {"id": "oai:u-ryukyu.repo.nii.ac.jp:02016141", "sets": ["1642838217169", "1642838412624"]}, "author_link": [], "item_1617186331708": {"attribute_name": "Title", "attribute_value_mlt": [{"subitem_1551255647225": "[\u7dcf\u8aac\uff3d\u8840\u7ba1\u5e73\u6ed1\u7b4bCa2^\u003c2+\u003e\u30c1\u30e3\u30cd\u30eb\u306e\u8abf\u7bc0\u6a5f\u69cb : \u30a2\u30af\u30c1\u30f3\u30d5\u30a3\u30e9\u30e1\u30f3\u30c8\u306e\u610f\u7fa9", "subitem_1551255648112": "ja"}, {"subitem_1551255647225": "Regulation of L-type Ca^\u003c2+\u003e channel activity in cultured vascular smooth muscle cells : the role of actin filament", "subitem_1551255648112": "en"}]}, "item_1617186419668": {"attribute_name": "Creator", "attribute_type": "creator", "attribute_value_mlt": [{"creatorNames": [{"creatorName": "\u4e2d\u6751, \u771f\u7406\u5b50", "creatorNameLang": "ja"}]}, {"creatorNames": [{"creatorName": "\u5c0f\u6749, \u5fe0\u8aa0", "creatorNameLang": "ja"}]}, {"creatorNames": [{"creatorName": "Nakamura, Mariko", "creatorNameLang": "en"}]}, {"creatorNames": [{"creatorName": "Kosugi, Tadayoshi", "creatorNameLang": "en"}]}]}, "item_1617186476635": {"attribute_name": "Access Rights", "attribute_value_mlt": [{"subitem_1522299639480": "open access", "subitem_1600958577026": "http://purl.org/coar/access_right/c_abf2"}]}, "item_1617186499011": {"attribute_name": "Rights", "attribute_value_mlt": [{"subitem_1522650717957": "ja", "subitem_1522651041219": "\u7409\u7403\u533b\u5b66\u4f1a"}]}, "item_1617186609386": {"attribute_name": "Subject", "attribute_value_mlt": [{"subitem_1522299896455": "en", "subitem_1522300014469": "Other", "subitem_1523261968819": "L-type Ca^\u003c2+\u003e channel"}, {"subitem_1522299896455": "en", "subitem_1522300014469": "Other", "subitem_1523261968819": "Actin filament"}, {"subitem_1522299896455": "en", "subitem_1522300014469": "Other", "subitem_1523261968819": "Vascular smooth muscle cells"}, {"subitem_1522299896455": "en", "subitem_1522300014469": "Other", "subitem_1523261968819": "Cytoskeleton"}, {"subitem_1522299896455": "en", "subitem_1522300014469": "Other", "subitem_1523261968819": "Colchicine"}]}, "item_1617186626617": {"attribute_name": "Description", "attribute_value_mlt": [{"subitem_description": "Changes in the cytoskeletal network alter the mechanical properties of cells that are essential for functions such as locomotion and cytokinesis. The transmembrane receptors and intracellular signals have been extensively studied on cytoskeletal changes in response to extracellular stimuli. After the procedure of percutaneous transluminal coronary angioplasty (PTCA) and highfrequency rotational atherectomy (PTCR) for stenosis of blood vessels, restenosis may be observed. The restenosis were generated under the proliferation and migration of vascular smooth muscle (VSM) cells. In addition, until recently it has been expected that the physiological regulation of VSM cells was dependent on L-type Ca^\u003c2+\u003e (Ca_1) channel activity and structure of the cytoskeleton. To clarify the interactions between the structure of the cytoskeleton and activity of Ca_1 channel in VSM cell, we used electrophysiological and morphological experiments concomitantly. We investigated the effect of disruption of the actin filaments and the microtubules on Ca_1 channel activity (Ca^\u003c2+\u003e current) of cultured VSM cells (A7r5 cell line) using whole cell voltage clamp. The results of immunostaining using anti-$ \\alpha $-actin and anti-$ \\alpha $-tubulin antibodies showed that colchicines disrupted both actin filaments and microtubules, while cytochalasin D and nocodazole disrupted only actin filaments, and microtubules respectively. Ca^\u003c2+\u003e current was greatly reduced in cells that were exposed to colchicines or cytochalasin D but not to nocodazole. When the actin filaments were stabilized by phalloidine, the inhibition of Ca^\u003c2+\u003e current was not observed. Actin filaments disruption of VSM cells inhibits Ca_1 channel activity, whereas the microtubules disruption gave no effect on the activity. These results suggested that the maintenance of physiological function in VSM cells involve the functional-structural relationship between the Ltype Ca^\u003c2+\u003e channel and cytoskeleton. The development of restenosis is dependent on the pathophysiological proliferation and then migration of the VSM cells could be prevented by control of L-type Ca^\u003c2+\u003e channel activity and stabilization of the cytoskeleton in VSM cells.", "subitem_description_type": "Other"}, {"subitem_description": "\u8ad6\u6587", "subitem_description_type": "Other"}]}, "item_1617186643794": {"attribute_name": "Publisher", "attribute_value_mlt": [{"subitem_1522300295150": "ja", "subitem_1522300316516": "\u7409\u7403\u533b\u5b66\u4f1a"}, {"subitem_1522300295150": "en", "subitem_1522300316516": "Ryukyu Medical Association"}]}, "item_1617186702042": {"attribute_name": "Language", "attribute_value_mlt": [{"subitem_1551255818386": "jpn"}]}, "item_1617186920753": {"attribute_name": "Source Identifier", "attribute_value_mlt": [{"subitem_1522646500366": "ISSN", "subitem_1522646572813": "1346888X"}, {"subitem_1522646500366": "ISSN", "subitem_1522646572813": "0289-1530"}, {"subitem_1522646500366": "NCID", "subitem_1522646572813": "AN10369445"}]}, "item_1617186941041": {"attribute_name": "Source Title", "attribute_value_mlt": [{"subitem_1522650068558": "ja", "subitem_1522650091861": "\u7409\u7403\u533b\u5b66\u4f1a\u8a8c = Ryukyu Medical Journal"}]}, "item_1617187056579": {"attribute_name": "Bibliographic Information", "attribute_value_mlt": [{"bibliographicIssueNumber": "1", "bibliographicPageEnd": "7", "bibliographicPageStart": "1", "bibliographicVolumeNumber": "21"}]}, "item_1617258105262": {"attribute_name": "Resource Type", "attribute_value_mlt": [{"resourcetype": "journal article", "resourceuri": "http://purl.org/coar/resource_type/c_6501"}]}, "item_1617265215918": {"attribute_name": "Version Type", "attribute_value_mlt": [{"subitem_1522305645492": "VoR", "subitem_1600292170262": "http://purl.org/coar/version/c_970fb48d4fbd8a85"}]}, "item_1617605131499": {"attribute_name": "File", "attribute_type": "file", "attribute_value_mlt": [{"accessrole": "open_access", "download_preview_message": "", "file_order": 0, "filename": "v21p1.pdf", "future_date_message": "", "is_thumbnail": false, "mimetype": "", "size": 0, "url": {"objectType": "fulltext", "url": "https://u-ryukyu.repo.nii.ac.jp/record/2016141/files/v21p1.pdf"}, "version_id": "8cd98bd3-d2ab-4a71-ad1a-aeb42575cb2c"}]}, "item_title": "[\u7dcf\u8aac\uff3d\u8840\u7ba1\u5e73\u6ed1\u7b4bCa2^\u003c2+\u003e\u30c1\u30e3\u30cd\u30eb\u306e\u8abf\u7bc0\u6a5f\u69cb : \u30a2\u30af\u30c1\u30f3\u30d5\u30a3\u30e9\u30e1\u30f3\u30c8\u306e\u610f\u7fa9", "item_type_id": "15", "owner": "1", "path": ["1642838217169", "1642838412624"], "permalink_uri": "http://hdl.handle.net/20.500.12000/0002016141", "pubdate": {"attribute_name": "PubDate", "attribute_value": "2010-07-02"}, "publish_date": "2010-07-02", "publish_status": "0", "recid": "2016141", "relation": {}, "relation_version_is_last": true, "title": ["[\u7dcf\u8aac\uff3d\u8840\u7ba1\u5e73\u6ed1\u7b4bCa2^\u003c2+\u003e\u30c1\u30e3\u30cd\u30eb\u306e\u8abf\u7bc0\u6a5f\u69cb : \u30a2\u30af\u30c1\u30f3\u30d5\u30a3\u30e9\u30e1\u30f3\u30c8\u306e\u610f\u7fa9"], "weko_shared_id": -1}
  1. 学術雑誌論文
  2. 琉球医学会
  3. 琉球医学会誌
  4. 21巻1号
  1. 部局別インデックス
  2. その他

[総説]血管平滑筋Ca2^<2+>チャネルの調節機構 : アクチンフィラメントの意義

http://hdl.handle.net/20.500.12000/0002016141
http://hdl.handle.net/20.500.12000/0002016141
e767cedd-ecb4-476f-8f21-a0ca0397c785
名前 / ファイル ライセンス アクション
v21p1.pdf v21p1.pdf
Item type デフォルトアイテムタイプ(フル)(1)
公開日 2010-07-02
タイトル
タイトル [総説]血管平滑筋Ca2^<2+>チャネルの調節機構 : アクチンフィラメントの意義
言語 ja
作成者 中村, 真理子

× 中村, 真理子

ja 中村, 真理子

小杉, 忠誠

× 小杉, 忠誠

ja 小杉, 忠誠

Nakamura, Mariko

× Nakamura, Mariko

en Nakamura, Mariko

Kosugi, Tadayoshi

× Kosugi, Tadayoshi

en Kosugi, Tadayoshi

アクセス権
アクセス権 open access
アクセス権URI http://purl.org/coar/access_right/c_abf2
権利情報
言語 ja
権利情報 琉球医学会
主題
言語 en
主題Scheme Other
主題 L-type Ca^<2+> channel
言語 en
主題Scheme Other
主題 Actin filament
言語 en
主題Scheme Other
主題 Vascular smooth muscle cells
言語 en
主題Scheme Other
主題 Cytoskeleton
言語 en
主題Scheme Other
主題 Colchicine
内容記述
内容記述タイプ Other
内容記述 Changes in the cytoskeletal network alter the mechanical properties of cells that are essential for functions such as locomotion and cytokinesis. The transmembrane receptors and intracellular signals have been extensively studied on cytoskeletal changes in response to extracellular stimuli. After the procedure of percutaneous transluminal coronary angioplasty (PTCA) and highfrequency rotational atherectomy (PTCR) for stenosis of blood vessels, restenosis may be observed. The restenosis were generated under the proliferation and migration of vascular smooth muscle (VSM) cells. In addition, until recently it has been expected that the physiological regulation of VSM cells was dependent on L-type Ca^<2+> (Ca_1) channel activity and structure of the cytoskeleton. To clarify the interactions between the structure of the cytoskeleton and activity of Ca_1 channel in VSM cell, we used electrophysiological and morphological experiments concomitantly. We investigated the effect of disruption of the actin filaments and the microtubules on Ca_1 channel activity (Ca^<2+> current) of cultured VSM cells (A7r5 cell line) using whole cell voltage clamp. The results of immunostaining using anti-$ \alpha $-actin and anti-$ \alpha $-tubulin antibodies showed that colchicines disrupted both actin filaments and microtubules, while cytochalasin D and nocodazole disrupted only actin filaments, and microtubules respectively. Ca^<2+> current was greatly reduced in cells that were exposed to colchicines or cytochalasin D but not to nocodazole. When the actin filaments were stabilized by phalloidine, the inhibition of Ca^<2+> current was not observed. Actin filaments disruption of VSM cells inhibits Ca_1 channel activity, whereas the microtubules disruption gave no effect on the activity. These results suggested that the maintenance of physiological function in VSM cells involve the functional-structural relationship between the Ltype Ca^<2+> channel and cytoskeleton. The development of restenosis is dependent on the pathophysiological proliferation and then migration of the VSM cells could be prevented by control of L-type Ca^<2+> channel activity and stabilization of the cytoskeleton in VSM cells.
内容記述タイプ Other
内容記述 論文
出版者
言語 ja
出版者 琉球医学会
言語
言語 jpn
資源タイプ
資源タイプ journal article
資源タイプ識別子 http://purl.org/coar/resource_type/c_6501
出版タイプ
出版タイプ VoR
出版タイプResource http://purl.org/coar/version/c_970fb48d4fbd8a85
収録物識別子
収録物識別子タイプ ISSN
収録物識別子 1346888X
収録物識別子タイプ ISSN
収録物識別子 0289-1530
収録物識別子タイプ NCID
収録物識別子 AN10369445
収録物名
言語 ja
収録物名 琉球医学会誌 = Ryukyu Medical Journal
書誌情報
巻 21, 号 1, p. 1-7
戻る
0
views
See details
Views

Versions

Ver.1 2022-02-22 04:15:08.813524
Show All versions

Share

Mendeley Twitter Facebook Print Addthis

Cite as

エクスポート

OAI-PMH
  • OAI-PMH JPCOAR
  • OAI-PMH DublinCore
  • OAI-PMH DDI
Other Formats
  • JSON

確認


Powered by WEKO3


Powered by WEKO3