DC Field | Value | Language |
dc.contributor.author | 陳錦澤 | zh_TW |
dc.creator | 陳錦澤 | zh_TW |
dc.date | 2000 | zh_TW |
dc.date.accessioned | 2006-07-26T03:19:45Z | - |
dc.date.accessioned | 2018-07-11T05:23:59Z | - |
dc.date.available | 2006-07-26T03:19:45Z | - |
dc.date.available | 2018-07-11T05:23:59Z | - |
dc.date.issued | 2000 | - |
dc.identifier | 892316B002028 | zh_TW |
dc.identifier.uri | http://ntur.lib.ntu.edu.tw//handle/246246/23520 | - |
dc.description.abstract | 內皮素會造成心肌細胞的肥大,而於
此過程中,心血管系統所釋放的一氧化氮
扮演著某種程度的對抗作用。本研究,在
於探討內生性一氧化氮對抗內皮素所誘發
c-fos 基因表現的作用機轉。實驗結果顯
示:內皮素經由活化其乙型接受器,會刺
激一氧化氮合成酵素,造成一氧化氮生成
增加。經由一氧化氮貢限劑如SNAP 、SIN-1
及一氧化氮清除劑PTIO 的運用,以北方式
點墨法搭配報告者基因轉染的方法,顯示
一氧化氮可對抗內皮素所誘發c-fos 的基因
表現;另外,以不同的負向突變基因Ras
(RasN17), Raf-1 (Raf301), 或mERK ,轉染
入心肌細胞皆可對抗內皮素所誘發c-fos 的
基因表現,顯示內皮素誘發c-fos 的基因表
現是經由Ras/Raf/ERK 的訊息路徑;直接
觀查一氧化氮對內皮素所激活ERK 的作
用,一氧化氮亦可對抗內皮素的激活ERK
的活性;猶有甚者,一氧化氮尚且可對抗
內皮素所增加乙型重鍊肌蛋白基因啟動子
活性的作用。縱合觀之,內皮素會造成心
肌細胞一氧化氮生成增加,而一氧化氮可
進一步對抗內皮素的激活ERK 的活性,造成對抗內皮素所誘發c-fos 的基因表現。 | zh_TW |
dc.description.abstract | Endothelin-1 (Et-1) treatment of cardiac
myocytes (CM) induces cardiac hypertrophy.
Cardiovascular release of nitric oxide (NO)
may play a role during cardiac hypertrophy.
The present study examined the protection
mechanism of endogenously released NO on
c-fos induction by Et-1 in neonatal rat CM.
CM exposed to Et-1 induced NO release. Et-1
stimulated nitric oxide synthase (NOS)
activity led to NO production that was
attenuated by treating CM with an antagonist
to endothelin B receptor. CM treated with a
NO donor, S-nitroso-N-acetylpenicillamine
(SNAP) or 3-morpholinosydnonimine (SIN-1),
inhibited Et-1–induced c-fos expression.
Conversely, CM treated with a NO scavenger,
2-phenyl-4,4,5,5,-tetramethyl-imidazoline-l-oxyl-
3-oxide (PTIO), augmented Et-1-induced
c-fos expression. The attenuation of
NO on c-fos expression was shown by
reducing either c-fos mRNA levels or c-fos
promoter activities using a chimera
containing the c-fos promoter region (-2.25
kb) ligated to a reporter gene CAT. In
contrast to the enhanced promoter activity in
CM after PTIO treatment, attenuated Et-1-induced
c-fos promoter activity was shown in
CM treated with a NO donor. CM
cotransfected with a dominant negative
mutant of Ras (RasN17), Raf-1 (Raf301), or
a catalytically inactive mutant of
extracellular signal–regulated kinase (ERK)–
2 (mERK) inhibited Et-1–induced c-fos
promoter activity, indicating Ras/Raf/ERK
pathway was involved. NO modulation of
this signaling pathway was shown by its
inhibitory effect on Et-1–induced ERK
activity. CM treated with NO resulted in a
decrease of Et-1-induced binding of nuclear
proteins to the AP-1 binding sequences.
Furthermore, CM treated with a NO donor
significantly suppressed Et-1-induced b-myosin
heavy chain promoter activities.
These results indicate that CM under Et-1
treatment increases NO levels and the
increased NO attenuated Et-1-induced c-fos
expression via the ERK signaling pathway.
These findings support the importance of NO
as a negative regulator in Et-1–induced gene
expression and cardiac hypertrophy. | en |
dc.format | application/pdf | zh_TW |
dc.format.extent | 333516 bytes | - |
dc.format.mimetype | application/pdf | - |
dc.language | zh-TW | zh_TW |
dc.language.iso | zh_TW | - |
dc.publisher | 臺北市:國立臺灣大學醫學院內科 | zh_TW |
dc.rights | 國立臺灣大學醫學院內科 | zh_TW |
dc.subject | 內皮素 | zh_TW |
dc.subject | 心肌細胞 | zh_TW |
dc.subject | 一氧化氮 | zh_TW |
dc.subject | Ras/Raf/ERK 訊息路徑 | zh_TW |
dc.subject | c-fos | zh_TW |
dc.subject | Endothelin-1 | en |
dc.subject | cardiomyocyte | en |
dc.subject | nitric oxide | en |
dc.subject | Ras//Raf/ERK signaling pathway | en |
dc.subject | c-fos | en |
dc.title | 一氧化氮與內皮素之間於新生鼠心臟細胞的交互作用 | zh_TW |
dc.type | report | en |
dc.identifier.uri.fulltext | http://ntur.lib.ntu.edu.tw/bitstream/246246/23520/1/892316B002028.pdf | - |
dc.coverage | 計畫年度:89
第一期;起迄日期:1999-08-01/2000-07-31 | zh_TW |
item.grantfulltext | open | - |
item.languageiso639-1 | zh_TW | - |
item.fulltext | with fulltext | - |
item.openairetype | report | - |
item.cerifentitytype | Publications | - |
item.openairecristype | http://purl.org/coar/resource_type/c_93fc | - |
Appears in Collections: | 醫學系
|