Calreticulin Protects Rat Microvascular Endothelial Cells against Microwave Radiation‐induced Injury by Attenuating Endoplasmic Reticulum Stress. (August 2014)
- Record Type:
- Journal Article
- Title:
- Calreticulin Protects Rat Microvascular Endothelial Cells against Microwave Radiation‐induced Injury by Attenuating Endoplasmic Reticulum Stress. (August 2014)
- Main Title:
- Calreticulin Protects Rat Microvascular Endothelial Cells against Microwave Radiation‐induced Injury by Attenuating Endoplasmic Reticulum Stress
- Authors:
- Li, Wei‐Hong
Li, Yu‐Zhen
Song, Dan‐Dan
Wang, Xiao‐Reng
Liu, Mi
Wu, Xu‐Dong
Liu, Xiu‐Hua - Abstract:
- <abstract abstract-type="main" id="micc12126-abs-0001"> <title>Abstract</title> <sec id="micc12126-sec-0001" sec-type="section"> <title>Objective</title> <p>This study was designed to evaluate whether exogenous CRT was beneficial for alleviating MR‐induced injury by suppressing ER stress in rat MMECs.</p> </sec> <sec id="micc12126-sec-0002" sec-type="section"> <title>Methods</title> <p>MMECs were pretreated with CRT (25 pg/mL) for 12 hours, followed by the exposure to 2.856 GHz radiation at a mean power density of 30 mW/cm<sup>2</sup> for six minutes. MR‐induced injury in MMECs was evaluated by LDH leakage, apoptosis, and cell viability analysis. The expression of GRP78, CRT, CHOP, Bcl‐2, and Bax were examined by Western blot analysis to reflect ER stress response and ER stress‐related apoptosis.</p> </sec> <sec id="micc12126-sec-0003" sec-type="section"> <title>Results</title> <p>MR induced marked MMECs injury, as shown by increased LDH leakage and apoptosis rate and decreased cell viability. MR also induced excessive ER stress, characterized by increased expression of GRP78 and CRT, and ER stress‐related apoptotic signaling as well, as shown by the upregulation of CHOP and Bax and the downregulation of Bcl‐2. Exogenous CRT pretreatment remarkably attenuated MR‐induced cell apoptosis and LDH leakage, ER stress, and activation of the ER stress‐related apoptotic signaling.</p> </sec> <sec id="micc12126-sec-0004" sec-type="section"> <title>Conclusions</title> <p>Exogenous CRT<abstract abstract-type="main" id="micc12126-abs-0001"> <title>Abstract</title> <sec id="micc12126-sec-0001" sec-type="section"> <title>Objective</title> <p>This study was designed to evaluate whether exogenous CRT was beneficial for alleviating MR‐induced injury by suppressing ER stress in rat MMECs.</p> </sec> <sec id="micc12126-sec-0002" sec-type="section"> <title>Methods</title> <p>MMECs were pretreated with CRT (25 pg/mL) for 12 hours, followed by the exposure to 2.856 GHz radiation at a mean power density of 30 mW/cm<sup>2</sup> for six minutes. MR‐induced injury in MMECs was evaluated by LDH leakage, apoptosis, and cell viability analysis. The expression of GRP78, CRT, CHOP, Bcl‐2, and Bax were examined by Western blot analysis to reflect ER stress response and ER stress‐related apoptosis.</p> </sec> <sec id="micc12126-sec-0003" sec-type="section"> <title>Results</title> <p>MR induced marked MMECs injury, as shown by increased LDH leakage and apoptosis rate and decreased cell viability. MR also induced excessive ER stress, characterized by increased expression of GRP78 and CRT, and ER stress‐related apoptotic signaling as well, as shown by the upregulation of CHOP and Bax and the downregulation of Bcl‐2. Exogenous CRT pretreatment remarkably attenuated MR‐induced cell apoptosis and LDH leakage, ER stress, and activation of the ER stress‐related apoptotic signaling.</p> </sec> <sec id="micc12126-sec-0004" sec-type="section"> <title>Conclusions</title> <p>Exogenous CRT attenuates MR‐induced ER stress‐related apoptosis by suppressing CHOP‐mediated apoptotic signaling pathways in MMECs.</p> </sec> </abstract> … (more)
- Is Part Of:
- Microcirculation. Volume 21:Number 6(2014:Aug.)
- Journal:
- Microcirculation
- Issue:
- Volume 21:Number 6(2014:Aug.)
- Issue Display:
- Volume 21, Issue 6 (2014)
- Year:
- 2014
- Volume:
- 21
- Issue:
- 6
- Issue Sort Value:
- 2014-0021-0006-0000
- Page Start:
- 506
- Page End:
- 515
- Publication Date:
- 2014-08
- Subjects:
- Biological transport -- Periodicals
Microcirculation -- Physiology -- Periodicals
612.135 - Journal URLs:
- http://onlinelibrary.wiley.com/journal/10.1111/(ISSN)1549-8719/issues ↗
http://onlinelibrary.wiley.com/ ↗
http://informahealthcare.com/loi/mic ↗ - DOI:
- 10.1111/micc.12126 ↗
- Languages:
- English
- ISSNs:
- 1073-9688
- Deposit Type:
- Legaldeposit
- View Content:
- Available online (eLD content is only available in our Reading Rooms) ↗
- Physical Locations:
- British Library DSC - 5758.460000
British Library DSC - BLDSS-3PM
British Library STI - ELD Digital store - Ingest File:
- 3441.xml