PMID- 38266580
OWN - NLM
STAT- MEDLINE
DCOM- 20240325
LR  - 20240328
IS  - 1878-7479 (Electronic)
IS  - 1933-7213 (Print)
IS  - 1878-7479 (Linking)
VI  - 21
IP  - 2
DP  - 2024 Mar
TI  - Pink1 deficiency enhances neurological deficits and inflammatory responses after 
      intracerebral hemorrhage in mice.
PG  - e00317
LID - S1878-7479(24)00003-5 [pii]
LID - 10.1016/j.neurot.2024.e00317 [doi]
LID - e00317
AB  - Pink1 (PTEN-induced putative kinase 1) is a protein associated with maintaining 
      mitochondrial function and integrity and has been reported to mediate 
      neurodegeneration and neuroinflammation. While the role of Pink1 in intracerebral 
      hemorrhage (ICH)-related neurological deficits and inflammatory responses is not 
      deciphered. Congenic blood was transfused into the left corpus striatum to 
      construct the ICH model in C57/BL6 wild-type (WT) and Pink1(-/-) mice. The 
      relative expression of Pink1, monocyte chemoattractant protein-1 (MCP-1), 
      macrophage inflammatory protein (MIP)-2, tumor necrosis factor (TNF)-alpha, 
      interleukin (IL)-1beta, Cd86, nitric oxide synthase 2 (Nos2), Cd206, arginase 1 
      (Arg-1), and IL-10 was detected with qRT-PCR, Western blotting, or ELISA. Mouse 
      neurological deficit scores (mNSS) and water content were detected, and an 
      open-field test was performed to assay anxiety-like behavior. Remarkably 
      decreased Pink1 expression and increased MIP-2, IL-1beta, MCP-1, and TNF-alpha 
      expression were observed after 12 ​h, 24 ​h, 48 ​h, 72 ​h, and 7 ​d post-ICH 
      induction in the ipsilateral injury hemispheres. Pink1 deficiency could further 
      up-regulate mNSS scores, brain water content, MIP-2, MCP-1, IL-1beta, and TNF-alpha in 
      the ipsilateral injury hemispheres. On the other hand, Pink1 deficiency could 
      decrease the number of center cross, the velocity, and the total distance 
      traveled in open field test. Pink1 deficiency could further up-regulate the mRNA 
      levels of pro-inflammatory (M1) molecules (Cd86, Nos2), and down-regulate the 
      relative expression of anti-inflammatory (M2) molecules (Cd206, Arg-1, and 
      IL-10). Pink1 deficiency deteriorates neurological deficits and inflammatory 
      responses after ICH, which can be considered as a treatment target.
CI  - Copyright (c) 2024 The Authors. Published by Elsevier Inc. All rights reserved.
FAU - Li, Jingchen
AU  - Li J
AD  - Department of Neurosurgery, The Second Hospital of Hebei Medical University, No. 
      215 Hepingxi Road, Shijiazhuang 050000, Hebei, China.
FAU - Li, Jianliang
AU  - Li J
AD  - Department of Neurosurgery, The Second Hospital of Hebei Medical University, No. 
      215 Hepingxi Road, Shijiazhuang 050000, Hebei, China.
FAU - Guo, Erkun
AU  - Guo E
AD  - Department of Neurosurgery, The Second Hospital of Hebei Medical University, No. 
      215 Hepingxi Road, Shijiazhuang 050000, Hebei, China.
FAU - Wang, Yuanyu
AU  - Wang Y
AD  - Department of Neurosurgery, The Second Hospital of Hebei Medical University, No. 
      215 Hepingxi Road, Shijiazhuang 050000, Hebei, China.
FAU - Yang, Ming
AU  - Yang M
AD  - Department of Neurosurgery, The Second Hospital of Hebei Medical University, No. 
      215 Hepingxi Road, Shijiazhuang 050000, Hebei, China.
FAU - Huo, Haoran
AU  - Huo H
AD  - Department of Neurosurgery, The Second Hospital of Hebei Medical University, No. 
      215 Hepingxi Road, Shijiazhuang 050000, Hebei, China.
FAU - Shi, Yunpeng
AU  - Shi Y
AD  - Department of Neurosurgery, The Second Hospital of Hebei Medical University, No. 
      215 Hepingxi Road, Shijiazhuang 050000, Hebei, China.
FAU - Zhao, Lin
AU  - Zhao L
AD  - Department of Neurosurgery, The Second Hospital of Hebei Medical University, No. 
      215 Hepingxi Road, Shijiazhuang 050000, Hebei, China. Electronic address: 
      zhaolin1973@126.com.
LA  - eng
PT  - Journal Article
DEP - 20240123
PL  - United States
TA  - Neurotherapeutics
JT  - Neurotherapeutics : the journal of the American Society for Experimental 
      NeuroTherapeutics
JID - 101290381
RN  - 130068-27-8 (Interleukin-10)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 059QF0KO0R (Water)
RN  - EC 2.7.11.1 (PTEN-induced putative kinase)
RN  - EC 2.7.- (Protein Kinases)
SB  - IM
MH  - Animals
MH  - Mice
MH  - Brain/metabolism
MH  - Cerebral Hemorrhage/complications/genetics/metabolism
MH  - *Interleukin-10
MH  - Mice, Inbred C57BL
MH  - *Tumor Necrosis Factor-alpha/metabolism
MH  - Water/metabolism
MH  - Protein Kinases/genetics/metabolism
PMC - PMC10963940
OTO - NOTNLM
OT  - Inflammation
OT  - Intracerebral hemorrhage
OT  - Neurological deficits
OT  - Pink1
COIS- Declaration of competing interest The authors declare that they have no known 
      competing financial interests or personal relationships that could have appeared 
      to influence the work reported in this paper.
EDAT- 2024/01/25 00:42
MHDA- 2024/03/25 06:43
PMCR- 2024/01/23
CRDT- 2024/01/24 18:34
PHST- 2023/11/11 00:00 [received]
PHST- 2023/12/30 00:00 [revised]
PHST- 2024/01/03 00:00 [accepted]
PHST- 2024/03/25 06:43 [medline]
PHST- 2024/01/25 00:42 [pubmed]
PHST- 2024/01/24 18:34 [entrez]
PHST- 2024/01/23 00:00 [pmc-release]
AID - S1878-7479(24)00003-5 [pii]
AID - e00317 [pii]
AID - 10.1016/j.neurot.2024.e00317 [doi]
PST - ppublish
SO  - Neurotherapeutics. 2024 Mar;21(2):e00317. doi: 10.1016/j.neurot.2024.e00317. Epub 
      2024 Jan 23.