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Title: Silencing MR-1 attenuates inflammatory damage in mice heart induced by AngII

Abstract

Myofibrillogenesis regulator-1(MR-1) can aggravate cardiac hypertrophy induced by angiotensin(Ang) II in mice through activation of NF-{kappa}B signaling pathway, and nuclear transcription factor (NF)-{kappa}B and activator protein-1(AP-1) regulate inflammatory and immune responses by increasing the expression of specific inflammatory genes in various tissues including heart. Whether inhibition of MR-1 expression will attenuate AngII-induced inflammatory injury in mice heart has not been explored. Herein, we monitored the activation of NF-{kappa}B and AP-1, together with expression of pro-inflammatory of interleukin(IL)-6, tumor necrosis factor(TNF)-{alpha}, vascular-cell adhesion molecule (VCAM)-1, platelet endothelial cell adhesion molecule (PECAM), and inflammatory cell infiltration in heart of mice which are induced firstly by AngII (PBS),then received MR-1-siRNA or control-siRNA injecting. We found that the activation of NF-{kappa}B and AP-1 was inhibited significantly, together with the decreased expression of IL-6, TNF-{alpha}, VCAM-1, and PECAM in AngII-induced mice myocardium in MR-1-siRNA injection groups compared with control-siRNA injecting groups. However, the expression level of MR-1 was not an apparent change in PBS-infused groups than in unoperation groups, and MR-1-siRNA do not affect the expression of MR-1 in PBS-infused mice. Our findings suggest that silencing MR-1 protected mice myocardium against inflammatory injury induced by AngII by suppression of pro-inflammatory transcription factors NF-{kappa}B and AP-1more » signaling pathway.« less

Authors:
 [1];  [2];  [1];  [1];  [1]
  1. Institute of Medicinal Biotechnology, Chinese Academy of Medical Sciences, Key Lab of Antibiotic Biotechnology, Ministry of Health, Beijing 100050 (China)
  2. Hunan Environment-Biological Polytechnic College, Hengyang Hunan 421005 (China)
Publication Date:
OSTI Identifier:
22202338
Resource Type:
Journal Article
Journal Name:
Biochemical and Biophysical Research Communications
Additional Journal Information:
Journal Volume: 391; Journal Issue: 3; Other Information: Copyright (c) 2009 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved.; Country of input: International Atomic Energy Agency (IAEA); Journal ID: ISSN 0006-291X
Country of Publication:
United States
Language:
English
Subject:
60 APPLIED LIFE SCIENCES; ANGIOTENSIN; ANIMAL TISSUES; HYPERTROPHY; INFLAMMATION; INJURIES; MICE; MYOCARDIUM; TRANSCRIPTION FACTORS

Citation Formats

Dai, Wenjian, Hunan Environment-Biological Polytechnic College, Hengyang Hunan 421005, Chen, Haiyang, Jiang, Jiandong, Kong, Weijia, and Wang, Yiguang. Silencing MR-1 attenuates inflammatory damage in mice heart induced by AngII. United States: N. p., 2010. Web. doi:10.1016/J.BBRC.2009.12.130.
Dai, Wenjian, Hunan Environment-Biological Polytechnic College, Hengyang Hunan 421005, Chen, Haiyang, Jiang, Jiandong, Kong, Weijia, & Wang, Yiguang. Silencing MR-1 attenuates inflammatory damage in mice heart induced by AngII. United States. https://doi.org/10.1016/J.BBRC.2009.12.130
Dai, Wenjian, Hunan Environment-Biological Polytechnic College, Hengyang Hunan 421005, Chen, Haiyang, Jiang, Jiandong, Kong, Weijia, and Wang, Yiguang. 2010. "Silencing MR-1 attenuates inflammatory damage in mice heart induced by AngII". United States. https://doi.org/10.1016/J.BBRC.2009.12.130.
@article{osti_22202338,
title = {Silencing MR-1 attenuates inflammatory damage in mice heart induced by AngII},
author = {Dai, Wenjian and Hunan Environment-Biological Polytechnic College, Hengyang Hunan 421005 and Chen, Haiyang and Jiang, Jiandong and Kong, Weijia and Wang, Yiguang},
abstractNote = {Myofibrillogenesis regulator-1(MR-1) can aggravate cardiac hypertrophy induced by angiotensin(Ang) II in mice through activation of NF-{kappa}B signaling pathway, and nuclear transcription factor (NF)-{kappa}B and activator protein-1(AP-1) regulate inflammatory and immune responses by increasing the expression of specific inflammatory genes in various tissues including heart. Whether inhibition of MR-1 expression will attenuate AngII-induced inflammatory injury in mice heart has not been explored. Herein, we monitored the activation of NF-{kappa}B and AP-1, together with expression of pro-inflammatory of interleukin(IL)-6, tumor necrosis factor(TNF)-{alpha}, vascular-cell adhesion molecule (VCAM)-1, platelet endothelial cell adhesion molecule (PECAM), and inflammatory cell infiltration in heart of mice which are induced firstly by AngII (PBS),then received MR-1-siRNA or control-siRNA injecting. We found that the activation of NF-{kappa}B and AP-1 was inhibited significantly, together with the decreased expression of IL-6, TNF-{alpha}, VCAM-1, and PECAM in AngII-induced mice myocardium in MR-1-siRNA injection groups compared with control-siRNA injecting groups. However, the expression level of MR-1 was not an apparent change in PBS-infused groups than in unoperation groups, and MR-1-siRNA do not affect the expression of MR-1 in PBS-infused mice. Our findings suggest that silencing MR-1 protected mice myocardium against inflammatory injury induced by AngII by suppression of pro-inflammatory transcription factors NF-{kappa}B and AP-1 signaling pathway.},
doi = {10.1016/J.BBRC.2009.12.130},
url = {https://www.osti.gov/biblio/22202338}, journal = {Biochemical and Biophysical Research Communications},
issn = {0006-291X},
number = 3,
volume = 391,
place = {United States},
year = {Fri Jan 15 00:00:00 EST 2010},
month = {Fri Jan 15 00:00:00 EST 2010}
}