PMID- 31591949
OWN - NLM
STAT- MEDLINE
DCOM- 20210324
LR  - 20210324
IS  - 1607-8888 (Electronic)
IS  - 1025-3890 (Linking)
VI  - 23
IP  - 3
DP  - 2020 May
TI  - Chronic restraint stress exacerbates neurological deficits and disrupts the 
      remodeling of the neurovascular unit in a mouse intracerebral hemorrhage model.
PG  - 338-348
LID - 10.1080/10253890.2019.1678023 [doi]
AB  - Growing evidences have shown that patients recovering from stroke experience high 
      and unremitting stress. Chronic restraint stress (CRS) has been found to 
      exacerbate neurological impairments in an experimental focal cortical ischemia 
      model. However, there have been no studies reporting the effect and mechanism of 
      CRS on intracerebral hemorrhage (ICH). This study aimed to evaluate the effect of 
      CRS on a mouse ICH model. Adult male C57BL mice were subjected to infusion of 
      collagenase IV (to induce ICH) or saline (for sham) into the left striatum. After 
      ICH, animals were stressed with application of CRS protocol for 21 days. Our 
      results showed that CRS significantly exacerbated neurological deficits (Garcia 
      test, corner turn test, and wire grip test) and the ipsilateral brain atrophy and 
      reduced body weight gain after ICH. Immunofluorescence staining indicated that 
      CRS exerted significant suppressive effects on neuron, astrocyte, vascular 
      endothelial cell and pericyte and excessively activated microglia post ICH. All 
      of the key cellular components mentioned above are involved in the neurovascular 
      unit (NVU) remodeling in the peri-hemorrhagic region after ICH. Western blot 
      results showed that matrix metalloproteinase (MMP)-9 and tight junction (TJ) 
      proteins including zonula occludens-1, occludin and claudin-5 were increased 
      after ICH, but MMP-9 protein was further up-regulated and TJ-related proteins 
      were down-regulated by CRS. In addition, ICH-induced activation of endoplasmic 
      reticulum stress and apoptosis were further strengthened by CRS. Collectively, 
      CRS exacerbates neurological deficits and disrupts the remodeling of the 
      peri-hemorrhagic NVU after ICH, which may be associated with TJ proteins 
      degradation and excessive activation of MMP-9 and endoplasmic reticulum 
      stress-apoptosis.LAY SUMMARYCRS exacerbates neurological deficits and disrupts 
      the remodeling of the NVU in the recovery stage after ICH, which suggest that 
      monitoring chronic stress levels in patients recovering from ICH may merit 
      consideration in the future.
FAU - Gao, Cheng
AU  - Gao C
AD  - Shanghai Key Laboratory of Forensic Medicine, Shanghai Forensic Service Platform, 
      Academy of Forensic Science, Shanghai, China.
AD  - Department of Forensic Medicine, Medical School of Soochow University, Suzhou, 
      China.
FAU - Meng, Ying
AU  - Meng Y
AD  - Community Health Center, Suzhou Western Eco-City, Suzhou, China.
FAU - Chen, Guang
AU  - Chen G
AD  - Department of Forensic Medicine, Medical School of Soochow University, Suzhou, 
      China.
FAU - Chen, Wei
AU  - Chen W
AD  - Department of Forensic Medicine, Medical School of Soochow University, Suzhou, 
      China.
FAU - Chen, Xue-Shi
AU  - Chen XS
AD  - Department of Forensic Medicine, Medical School of Soochow University, Suzhou, 
      China.
FAU - Luo, Cheng-Liang
AU  - Luo CL
AD  - Department of Forensic Medicine, Medical School of Soochow University, Suzhou, 
      China.
FAU - Zhang, Ming-Yang
AU  - Zhang MY
AD  - Department of Forensic Medicine, Medical School of Soochow University, Suzhou, 
      China.
FAU - Wang, Zu-Feng
AU  - Wang ZF
AD  - Department of Forensic Medicine, Medical School of Soochow University, Suzhou, 
      China.
FAU - Wang, Tao
AU  - Wang T
AD  - Shanghai Key Laboratory of Forensic Medicine, Shanghai Forensic Service Platform, 
      Academy of Forensic Science, Shanghai, China.
AD  - Department of Forensic Medicine, Medical School of Soochow University, Suzhou, 
      China.
AD  - School of Pharmacy, Soochow University, Suzhou, China.
FAU - Tao, Lu-Yang
AU  - Tao LY
AD  - Department of Forensic Medicine, Medical School of Soochow University, Suzhou, 
      China.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20191018
PL  - England
TA  - Stress
JT  - Stress (Amsterdam, Netherlands)
JID - 9617529
SB  - IM
MH  - Animals
MH  - *Cerebral Hemorrhage
MH  - Disease Models, Animal
MH  - Humans
MH  - Male
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Neurons
MH  - *Stress, Psychological
OTO - NOTNLM
OT  - Intracerebral hemorrhage
OT  - apoptosis
OT  - chronic restraint stress
OT  - endoplasmic reticulum stress
OT  - neurovascular unit
OT  - tight junction
EDAT- 2019/10/09 06:00
MHDA- 2021/03/25 06:00
CRDT- 2019/10/09 06:00
PHST- 2019/10/09 06:00 [pubmed]
PHST- 2021/03/25 06:00 [medline]
PHST- 2019/10/09 06:00 [entrez]
AID - 10.1080/10253890.2019.1678023 [doi]
PST - ppublish
SO  - Stress. 2020 May;23(3):338-348. doi: 10.1080/10253890.2019.1678023. Epub 2019 Oct 
      18.