PMID- 33090046
OWN - NLM
STAT- MEDLINE
DCOM- 20210512
LR  - 20211204
IS  - 1557-8682 (Electronic)
IS  - 1527-0297 (Linking)
VI  - 21
IP  - 4
DP  - 2020 Dec
TI  - Oxidative and Endoplasmic Reticulum Stress Responses to Chronic High-Altitude 
      Exposure During the Development of High-Altitude Pulmonary Hypertension.
PG  - 378-387
LID - 10.1089/ham.2019.0143 [doi]
AB  - Pu, Xiaoyan, Xue Lin, Xianglan Duan, Junjie Wang, Jun Shang, Haixia Yun, and Zhi 
      Chen. Oxidative and endoplasmic reticulum stress responses to chronic 
      high-altitude exposure during the development of high-altitude pulmonary 
      hypertension. High Alt Med Biol. 21:378-387, 2020. Objectives: To investigate the 
      effect of endoplasmic reticulum (ER) stress during the development of 
      high-altitude pulmonary hypertension (HAPH) after chronic high-altitude exposure, 
      as well as the association between oxidative stress and ER stress. Methods: Forty 
      male Sprague-Dawley rats were placed in a low-pressure chamber with a simulated 
      altitude of 4,200 m for 0-28 days. Rats were chosen at random on days 0, 7, 14, 
      and 28 of chronic high-altitude exposure and were examined for pulmonary arterial 
      pressure, oxidative stress, apoptosis, and ER stress. Results: Chronic 
      high-altitude exposure caused a continuous deterioration of pulmonary 
      hypertension, which was accompanied by obvious apoptosis of alveolar epithelial 
      cells and remodeling of pulmonary vessels. From day 7 of high-altitude exposure, 
      although the activities of glutathione peroxidase and superoxide dismutase were 
      gradually decreased, the generation of both malondialdehyde and reactive oxygen 
      species was increased in a time-dependent manner. The protein expression of ER 
      stress-related GRP78, PERK, IRE1alpha, ATF6, ATF4, CHOP, and caspase-12 in lung 
      tissue was significantly upregulated from day 14 of high-altitude exposure. 
      Further, the expression of caspase-12 in alveolar epithelial cells and vascular 
      smooth muscle cells was also increased from day 14 of high-altitude exposure. 
      Conclusions: Early high-altitude exposure first activates oxidative stress; then, 
      it gradually activates ER stress. The activation of ER stress might promote the 
      apoptosis of alveolar epithelial cells and the remodeling of pulmonary vessels by 
      exacerbating the oxidative stress response during the development of HAPH after 
      chronic high-altitude exposure.
FAU - Pu, Xiaoyan
AU  - Pu X
AD  - School of Life Science, Qinghai Normal University, Xining, China.
AD  - Medical College, Qinghai University, Xining, China.
FAU - Lin, Xue
AU  - Lin X
AD  - Medical College, Qinghai University, Xining, China.
FAU - Duan, Xianglan
AU  - Duan X
AD  - School of Life Science, Qinghai Normal University, Xining, China.
FAU - Wang, Junjie
AU  - Wang J
AD  - School of Life Science, Qinghai Normal University, Xining, China.
FAU - Shang, Jun
AU  - Shang J
AD  - School of Life Science, Qinghai Normal University, Xining, China.
FAU - Yun, Haixia
AU  - Yun H
AD  - School of Life Science, Qinghai Normal University, Xining, China.
FAU - Chen, Zhi
AU  - Chen Z
AD  - School of Life Science, Qinghai Normal University, Xining, China.
LA  - eng
PT  - Journal Article
DEP - 20201021
PL  - United States
TA  - High Alt Med Biol
JT  - High altitude medicine & biology
JID - 100901183
RN  - EC 2.7.11.1 (Protein Serine-Threonine Kinases)
RN  - EC 3.1.- (Endoribonucleases)
SB  - IM
MH  - Altitude
MH  - Animals
MH  - Apoptosis
MH  - *Endoplasmic Reticulum Stress
MH  - Endoribonucleases
MH  - *Hypertension, Pulmonary/etiology
MH  - Male
MH  - Oxidative Stress
MH  - Protein Serine-Threonine Kinases
MH  - Rats
MH  - Rats, Sprague-Dawley
OTO - NOTNLM
OT  - apoptosis
OT  - chronic high-altitude exposure
OT  - endoplasmic reticulum
OT  - high-altitude pulmonary hypertension
OT  - oxidative stress
OT  - pulmonary vessels remodeling
EDAT- 2020/10/23 06:00
MHDA- 2021/05/13 06:00
CRDT- 2020/10/22 12:15
PHST- 2020/10/23 06:00 [pubmed]
PHST- 2021/05/13 06:00 [medline]
PHST- 2020/10/22 12:15 [entrez]
AID - 10.1089/ham.2019.0143 [doi]
PST - ppublish
SO  - High Alt Med Biol. 2020 Dec;21(4):378-387. doi: 10.1089/ham.2019.0143. Epub 2020 
      Oct 21.