PMID- 37331689
OWN - NLM
STAT- MEDLINE
DCOM- 20230816
LR  - 20230817
IS  - 1873-7544 (Electronic)
IS  - 0306-4522 (Linking)
VI  - 526
DP  - 2023 Aug 21
TI  - Hypoxic Postconditioning Promotes Angiogenesis After Ischemic Stroke.
PG  - 35-47
LID - S0306-4522(23)00265-8 [pii]
LID - 10.1016/j.neuroscience.2023.06.009 [doi]
AB  - Although hypoxic postconditioning (HPC) has a protective effect on ischemic 
      stroke, its effect on angiogenesis after ischemic stroke is still unclear. This 
      study was designed to investigate the effects of HPC on angiogenesis after 
      ischemic stroke and to preliminarily study the mechanism involved. Oxygen-glucose 
      deprivation (OGD)-intervened bEnd.3 (mouse brain-derived Endothelial cell. 3) was 
      used to simulate cerebral ischemia. Cell counting kit-8 (CCK-8), Cell BrdU 
      proliferation, wound healing, Transwell and tube formation assays were used to 
      evaluate the effect of HPC on the cell viability, proliferation, migration 
      (horizontal and vertical migration), morphogenesis and tube formation of bEnd.3. 
      A middle cerebral artery occlusion (MCAO) model was made in C57 mice to simulate 
      focal cerebral ischemia. Rod rotation test, corner test, modified neurological 
      severity score (mNSS), and balance beam walking test were used to evaluate the 
      effect of HPC on the neurological impairment of mice. Immunofluorescence staining 
      was used to evaluate the effect of HPC on angiogenesis in mice. The 
      angiogenesis-related proteins were evaluated and quantified using western blot. 
      Results showed that HPC significantly promoted proliferation, migration and tube 
      formation of bEnd.3. HPC significantly reversed the neurological deficit of MCAO 
      mice. Moreover, HPC significantly promoted angiogenesis in the peri-infarct area, 
      and angiogenesis was found to be positively correlated with the improvement of 
      neurological impairment. The HPC mice showed higher PLClambda and ALK5 than did MCAO. 
      We conclude that HPC improves the neurological deficit caused by focal cerebral 
      ischemia by promoting angiogenesis. Furthermore, the effect of HPC on improving 
      angiogenesis may be related to PLClambda and ALK5.
CI  - Copyright (c) 2023 IBRO. Published by Elsevier Ltd. All rights reserved.
FAU - Shi, Wenjie
AU  - Shi W
AD  - North China University of Science and Technology Affiliated Hospital, Tangshan 
      063000, China; Beijing Key Laboratory of Hypoxia Translational Medicine, Xuanwu 
      Hospital, Capital Medical University, Beijing 100053, China.
FAU - Ren, Changhong
AU  - Ren C
AD  - Beijing Key Laboratory of Hypoxia Translational Medicine, Xuanwu Hospital, 
      Capital Medical University, Beijing 100053, China; Center of Stroke, Beijing 
      Institute for Brain Disorder, Capital Medical University, Beijing 100053, China.
FAU - Zhang, Wei
AU  - Zhang W
AD  - Beijing Key Laboratory of Hypoxia Translational Medicine, Xuanwu Hospital, 
      Capital Medical University, Beijing 100053, China.
FAU - Gao, Chen
AU  - Gao C
AD  - Beijing Key Laboratory of Hypoxia Translational Medicine, Xuanwu Hospital, 
      Capital Medical University, Beijing 100053, China.
FAU - Yu, Wantong
AU  - Yu W
AD  - Beijing Key Laboratory of Hypoxia Translational Medicine, Xuanwu Hospital, 
      Capital Medical University, Beijing 100053, China.
FAU - Ji, Xunming
AU  - Ji X
AD  - Beijing Key Laboratory of Hypoxia Translational Medicine, Xuanwu Hospital, 
      Capital Medical University, Beijing 100053, China; Center of Stroke, Beijing 
      Institute for Brain Disorder, Capital Medical University, Beijing 100053, China.
FAU - Chang, Lisha
AU  - Chang L
AD  - North China University of Science and Technology Affiliated Hospital, Tangshan 
      063000, China. Electronic address: clsha1975@163.com.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20230616
PL  - United States
TA  - Neuroscience
JT  - Neuroscience
JID - 7605074
SB  - IM
MH  - Mice
MH  - Animals
MH  - *Ischemic Stroke
MH  - *Brain Ischemia/metabolism
MH  - Infarction, Middle Cerebral Artery
MH  - Morphogenesis
MH  - *Stroke/metabolism
MH  - *Ischemic Postconditioning
OTO - NOTNLM
OT  - angiogenesis
OT  - hypoxic postconditioning
OT  - ischemic stroke
OT  - neuroprotection
EDAT- 2023/06/19 00:42
MHDA- 2023/08/16 06:43
CRDT- 2023/06/18 19:18
PHST- 2023/02/12 00:00 [received]
PHST- 2023/06/08 00:00 [revised]
PHST- 2023/06/12 00:00 [accepted]
PHST- 2023/08/16 06:43 [medline]
PHST- 2023/06/19 00:42 [pubmed]
PHST- 2023/06/18 19:18 [entrez]
AID - S0306-4522(23)00265-8 [pii]
AID - 10.1016/j.neuroscience.2023.06.009 [doi]
PST - ppublish
SO  - Neuroscience. 2023 Aug 21;526:35-47. doi: 10.1016/j.neuroscience.2023.06.009. 
      Epub 2023 Jun 16.