PMID- 31588926
OWN - NLM
STAT- MEDLINE
DCOM- 20200309
LR  - 20211224
IS  - 1643-3750 (Electronic)
IS  - 1234-1010 (Print)
IS  - 1234-1010 (Linking)
VI  - 25
DP  - 2019 Oct 7
TI  - Aggravation of Cerebral Ischemia/Reperfusion Injury by Peroxisome 
      Proliferator-Activated Receptor-Gamma Deficiency via Endoplasmic Reticulum 
      Stress.
PG  - 7518-7526
LID - 10.12659/MSM.915914 [doi]
AB  - BACKGROUND Ischemic stroke is a dominant contributor to disability and mortality 
      worldwide and is recognized as an important health concern. As a transcription 
      factor triggered via stress, peroxisome proliferator-activated receptor-gamma 
      (PPAR-gamma) has a crucial impact on differentiation, cell death, and cell growth. 
      However, the role of PPAR-gamma and its precise mechanism in cerebral ischemia injury 
      (CII) remain unclear. MATERIAL AND METHODS The male C57Bl/6 mice (12 weeks old, 
      n=52) were subjected to middle cerebral artery occlusion (MCAO). Infarct volume 
      was evaluated by 2, 3, 5-Triphenyltetrazolium chloride staining. Cell apoptosis 
      was measured by terminal dUTP nick-end labeling (TUNEL) staining. The expression 
      of apoptotic-related protein was examined by Western blotting. Neuron2A cells 
      were transfected with PPAR-gamma-specific siRNA and then were subjected to 
      oxygen-glucose exhaustion and reoxygenation. RESULTS It was observed that 
      PPAR-gamma-deficient mice displayed extended infarct trigon in the MCAO stroke model. 
      Neuronal deficiency was more severe in PPAR-gamma-deficient models. Additionally, 
      expression of cell death-promoting Bcl-2 associated X and active caspase-3 was 
      reinforced, while that of cell death-counteracting Bcl-2 was repressed in 
      PPAR-gamma-deficient mice. This was characterized by reinforced endoplasmic reticulum 
      (ER) stress reactions in in vivo brain specimens as well as in vitro neurons in 
      ischemia/reperfusion (I/R) injury. CONCLUSIONS This research proved that PPAR-gamma 
      protected the brain from cerebral I/R injury by repressing ER stress and 
      indicated that PPAR-gamma is a potential target in the treatment of ischemia.
FAU - Chen, Yueping
AU  - Chen Y
AD  - Clinical Laboratory, The Third Affiliated Hospital of Wenzhou Medical University, 
      Ruian, Zhejiang, China (mainland).
FAU - Liu, Shihui
AU  - Liu S
AD  - Department of Neurology, Linyi Central Hospital, Linyi, Shandong, China 
      (mainland).
FAU - Chen, Guangyong
AU  - Chen G
AD  - Department of Neurology, The Third Affiliated Hospital of Wenzhou Medical 
      University, Ruian, Zhejiang, China (mainland).
LA  - eng
PT  - Journal Article
PT  - Retracted Publication
DEP - 20191007
PL  - United States
TA  - Med Sci Monit
JT  - Medical science monitor : international medical journal of experimental and 
      clinical research
JID - 9609063
RN  - 0 (PPAR gamma)
SB  - IM
RIN - Med Sci Monit. 2021 Nov 01;28:e935290. PMID: 34719667
MH  - Animals
MH  - Apoptosis/physiology
MH  - Brain/metabolism
MH  - Brain Ischemia/*metabolism/pathology
MH  - Disease Models, Animal
MH  - Endoplasmic Reticulum/physiology
MH  - Endoplasmic Reticulum Stress/physiology
MH  - Infarction, Middle Cerebral Artery/metabolism
MH  - Male
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Neurons/metabolism
MH  - PPAR gamma/*metabolism
MH  - Reperfusion Injury/*metabolism/pathology
MH  - Stroke/metabolism
PMC - PMC6792513
EDAT- 2019/10/08 06:00
MHDA- 2020/03/10 06:00
PMCR- 2019/10/07
CRDT- 2019/10/08 06:00
PHST- 2019/10/08 06:00 [entrez]
PHST- 2019/10/08 06:00 [pubmed]
PHST- 2020/03/10 06:00 [medline]
PHST- 2019/10/07 00:00 [pmc-release]
AID - 915914 [pii]
AID - 10.12659/MSM.915914 [doi]
PST - epublish
SO  - Med Sci Monit. 2019 Oct 7;25:7518-7526. doi: 10.12659/MSM.915914.