Induction of Apoptosis by Hypertension Via Endoplasmic Reticulum Stress

Background/Aims: Endoplasmic reticulum (ER) stress is one of the intrinsic apoptosis pathways, and cardiac apoptosis can occur in cardiovascular diseases, such as hypertension. However, the mechanisms by which ER stress leads to apoptosis remain enigmatic, particularly in the progression from cardia...

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Main Authors: Yingying Sun, Tong Zhang, Li Li, Ji Wang
Format: Article
Language:English
Published: Karger Publishers 2015-02-01
Series:Kidney & Blood Pressure Research
Subjects:
Online Access:http://www.karger.com/Article/FullText/368481
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author Yingying Sun
Tong Zhang
Li Li
Ji Wang
author_facet Yingying Sun
Tong Zhang
Li Li
Ji Wang
author_sort Yingying Sun
collection DOAJ
description Background/Aims: Endoplasmic reticulum (ER) stress is one of the intrinsic apoptosis pathways, and cardiac apoptosis can occur in cardiovascular diseases, such as hypertension. However, the mechanisms by which ER stress leads to apoptosis remain enigmatic, particularly in the progression from cardiac hypertrophy to diastolic heart failure due to hypertension. Methods: We used spontaneously hypertensive rats (SHRs) to investigate possible signalling pathways for ER stress. Results: We found that cardiac protein and mRNA levels of glucose-regulated protein 78 were up-regulated. In addition, the CHOP- and caspase-12-dependent pathways, but not that of JNK, were activated in the SHR rats. Conclusions: These results suggest that ER stress can contribute to myocardial apoptosis during hypertensive disease.
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spelling doaj.art-0c6b801d2d08434abe05cd6745862b692022-12-21T23:07:09ZengKarger PublishersKidney & Blood Pressure Research1420-40961423-01432015-02-01401415110.1159/000368481368481Induction of Apoptosis by Hypertension Via Endoplasmic Reticulum StressYingying SunTong ZhangLi LiJi WangBackground/Aims: Endoplasmic reticulum (ER) stress is one of the intrinsic apoptosis pathways, and cardiac apoptosis can occur in cardiovascular diseases, such as hypertension. However, the mechanisms by which ER stress leads to apoptosis remain enigmatic, particularly in the progression from cardiac hypertrophy to diastolic heart failure due to hypertension. Methods: We used spontaneously hypertensive rats (SHRs) to investigate possible signalling pathways for ER stress. Results: We found that cardiac protein and mRNA levels of glucose-regulated protein 78 were up-regulated. In addition, the CHOP- and caspase-12-dependent pathways, but not that of JNK, were activated in the SHR rats. Conclusions: These results suggest that ER stress can contribute to myocardial apoptosis during hypertensive disease.http://www.karger.com/Article/FullText/368481ApoptosisCaspase-12CHOPER stressGRP78Hypertension
spellingShingle Yingying Sun
Tong Zhang
Li Li
Ji Wang
Induction of Apoptosis by Hypertension Via Endoplasmic Reticulum Stress
Kidney & Blood Pressure Research
Apoptosis
Caspase-12
CHOP
ER stress
GRP78
Hypertension
title Induction of Apoptosis by Hypertension Via Endoplasmic Reticulum Stress
title_full Induction of Apoptosis by Hypertension Via Endoplasmic Reticulum Stress
title_fullStr Induction of Apoptosis by Hypertension Via Endoplasmic Reticulum Stress
title_full_unstemmed Induction of Apoptosis by Hypertension Via Endoplasmic Reticulum Stress
title_short Induction of Apoptosis by Hypertension Via Endoplasmic Reticulum Stress
title_sort induction of apoptosis by hypertension via endoplasmic reticulum stress
topic Apoptosis
Caspase-12
CHOP
ER stress
GRP78
Hypertension
url http://www.karger.com/Article/FullText/368481
work_keys_str_mv AT yingyingsun inductionofapoptosisbyhypertensionviaendoplasmicreticulumstress
AT tongzhang inductionofapoptosisbyhypertensionviaendoplasmicreticulumstress
AT lili inductionofapoptosisbyhypertensionviaendoplasmicreticulumstress
AT jiwang inductionofapoptosisbyhypertensionviaendoplasmicreticulumstress