Molecular mechanism of (-)-epigallocatechin-3-gallate on balloon injury-induced neointimal formation and leptin expression

Chiu Mei Lin, Sheng Wen Hou, Bao Wei Wang, Jiann Ruey Ong, Hang Chang, Kou-Gi Shyu

研究成果: 雜誌貢獻文章

6 引文 (Scopus)

摘要

Leptin contributes to the pathogenesis of vascular repair and cardiovascular events. This study evaluated the molecular mechanism of EGCG in balloon injury-induced leptin expression. According to immunohistochemical and confocal analyses, leptin expression was increased and the aortic lumen exhibited narrowing after balloon injury. EGCG treatment attenuated leptin expression and diminished neointimal formation. The in vitro study showed that angiotensin II (Ang II) induced the migration and proliferation of cultured vascular smooth muscle cells (VSMCs), whereas treatment with EGCG, leptin siRNA, and c-Jun siRNA inhibited the migration and proliferation of VSMCs significantly. The EMSA shows that balloon injury increased AP-1-binding activity, and EGCG and c-Jun siRNA inhibited the AP-1-binding activity. Western blot and real-time RT-PCR analyses revealed similar results in intimal tissue samples. In summary, balloon injury induces leptin expression in the carotid artery of rats, and EGCG inhibits leptin expression through the JNK/AP-1 pathway and also attenuates neointimal formation.
原文英語
頁(從 - 到)1213-1220
頁數8
期刊Journal of Agricultural and Food Chemistry
62
發行號6
DOIs
出版狀態已發佈 - 二月 12 2014

指紋

epigallocatechin
Balloons
Leptin
leptin
Wounds and Injuries
Transcription Factor AP-1
small interfering RNA
blood vessels
Small Interfering RNA
Vascular Smooth Muscle
smooth muscle
myocytes
Smooth Muscle Myocytes
Muscle
Tunica Intima
angiotensin II
carotid arteries
epigallocatechin gallate
Carotid Arteries
Angiotensin II

ASJC Scopus subject areas

  • Agricultural and Biological Sciences(all)
  • Chemistry(all)

引用此文

Molecular mechanism of (-)-epigallocatechin-3-gallate on balloon injury-induced neointimal formation and leptin expression. / Lin, Chiu Mei; Hou, Sheng Wen; Wang, Bao Wei; Ong, Jiann Ruey; Chang, Hang; Shyu, Kou-Gi.

於: Journal of Agricultural and Food Chemistry, 卷 62, 編號 6, 12.02.2014, p. 1213-1220.

研究成果: 雜誌貢獻文章

Lin, Chiu Mei ; Hou, Sheng Wen ; Wang, Bao Wei ; Ong, Jiann Ruey ; Chang, Hang ; Shyu, Kou-Gi. / Molecular mechanism of (-)-epigallocatechin-3-gallate on balloon injury-induced neointimal formation and leptin expression. 於: Journal of Agricultural and Food Chemistry. 2014 ; 卷 62, 編號 6. 頁 1213-1220.
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abstract = "Leptin contributes to the pathogenesis of vascular repair and cardiovascular events. This study evaluated the molecular mechanism of EGCG in balloon injury-induced leptin expression. According to immunohistochemical and confocal analyses, leptin expression was increased and the aortic lumen exhibited narrowing after balloon injury. EGCG treatment attenuated leptin expression and diminished neointimal formation. The in vitro study showed that angiotensin II (Ang II) induced the migration and proliferation of cultured vascular smooth muscle cells (VSMCs), whereas treatment with EGCG, leptin siRNA, and c-Jun siRNA inhibited the migration and proliferation of VSMCs significantly. The EMSA shows that balloon injury increased AP-1-binding activity, and EGCG and c-Jun siRNA inhibited the AP-1-binding activity. Western blot and real-time RT-PCR analyses revealed similar results in intimal tissue samples. In summary, balloon injury induces leptin expression in the carotid artery of rats, and EGCG inhibits leptin expression through the JNK/AP-1 pathway and also attenuates neointimal formation.",
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AU - Hou, Sheng Wen

AU - Wang, Bao Wei

AU - Ong, Jiann Ruey

AU - Chang, Hang

AU - Shyu, Kou-Gi

PY - 2014/2/12

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N2 - Leptin contributes to the pathogenesis of vascular repair and cardiovascular events. This study evaluated the molecular mechanism of EGCG in balloon injury-induced leptin expression. According to immunohistochemical and confocal analyses, leptin expression was increased and the aortic lumen exhibited narrowing after balloon injury. EGCG treatment attenuated leptin expression and diminished neointimal formation. The in vitro study showed that angiotensin II (Ang II) induced the migration and proliferation of cultured vascular smooth muscle cells (VSMCs), whereas treatment with EGCG, leptin siRNA, and c-Jun siRNA inhibited the migration and proliferation of VSMCs significantly. The EMSA shows that balloon injury increased AP-1-binding activity, and EGCG and c-Jun siRNA inhibited the AP-1-binding activity. Western blot and real-time RT-PCR analyses revealed similar results in intimal tissue samples. In summary, balloon injury induces leptin expression in the carotid artery of rats, and EGCG inhibits leptin expression through the JNK/AP-1 pathway and also attenuates neointimal formation.

AB - Leptin contributes to the pathogenesis of vascular repair and cardiovascular events. This study evaluated the molecular mechanism of EGCG in balloon injury-induced leptin expression. According to immunohistochemical and confocal analyses, leptin expression was increased and the aortic lumen exhibited narrowing after balloon injury. EGCG treatment attenuated leptin expression and diminished neointimal formation. The in vitro study showed that angiotensin II (Ang II) induced the migration and proliferation of cultured vascular smooth muscle cells (VSMCs), whereas treatment with EGCG, leptin siRNA, and c-Jun siRNA inhibited the migration and proliferation of VSMCs significantly. The EMSA shows that balloon injury increased AP-1-binding activity, and EGCG and c-Jun siRNA inhibited the AP-1-binding activity. Western blot and real-time RT-PCR analyses revealed similar results in intimal tissue samples. In summary, balloon injury induces leptin expression in the carotid artery of rats, and EGCG inhibits leptin expression through the JNK/AP-1 pathway and also attenuates neointimal formation.

KW - angiotensin II

KW - balloon injury

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