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Evaluation of Connexin 43 Redistribution and Endocytosis in Astrocytes Subjected to Ischemia/Reperfusion or Oxygen-Glucose Deprivation and Reoxygenation.

Abstract Connexin 43 (Cx43) is the major component protein in astrocytic gap junction communication. Recent studies have shown the cellular processes of gap junction internalization and degradation, but many details remain unknown. This study investigated the distribution of Cx43 and its mechanism after ischemic insult. Astrocyte culture system and a model of ischemia/reperfusion (IR) or oxygen-glucose deprivation and reoxygenation (OGDR) were established. Cx43 distribution was observed by laser scanning confocal microscopy under different cultivation conditions. Western blot and RT-PCR assays were applied to quantify Cx43 and MAPRE1 (microtubule-associated protein RP/EB family member 1) expression at different time points. The total number of Cx43 was unchanged in the normal and IR/OGDR groups, but Cx43 particles in the cytoplasm of the IR/OGDR group were significantly greater than that of the normal group. Particles in the cytoplasm were significantly fewer after endocytosis was blocked by dynasore. There was no difference among the groups at each time point regarding protein or gene expression of MAPRE1. We concluded that internalization of Cx43 into the cytoplasm occurred during ischemia, which was partially mediated through endocytosis, not by the change of Cx43 quantity. Moreover, internalization was not related to microtubule transport.
PMID
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Authors

Mayor MeshTerms
Keywords
Journal Title biomed research international
Publication Year Start




PMID- 28424784
OWN - NLM
STAT- In-Process
DA  - 20170420
LR  - 20170423
IS  - 2314-6141 (Electronic)
VI  - 2017
DP  - 2017
TI  - Evaluation of Connexin 43 Redistribution and Endocytosis in Astrocytes Subjected 
      to Ischemia/Reperfusion or Oxygen-Glucose Deprivation and Reoxygenation.
PG  - 5064683
LID - 10.1155/2017/5064683 [doi]
AB  - Connexin 43 (Cx43) is the major component protein in astrocytic gap junction
      communication. Recent studies have shown the cellular processes of gap junction
      internalization and degradation, but many details remain unknown. This study
      investigated the distribution of Cx43 and its mechanism after ischemic insult.
      Astrocyte culture system and a model of ischemia/reperfusion (IR) or
      oxygen-glucose deprivation and reoxygenation (OGDR) were established. Cx43
      distribution was observed by laser scanning confocal microscopy under different
      cultivation conditions. Western blot and RT-PCR assays were applied to quantify
      Cx43 and MAPRE1 (microtubule-associated protein RP/EB family member 1) expression
      at different time points. The total number of Cx43 was unchanged in the normal
      and IR/OGDR groups, but Cx43 particles in the cytoplasm of the IR/OGDR group were
      significantly greater than that of the normal group. Particles in the cytoplasm
      were significantly fewer after endocytosis was blocked by dynasore. There was no 
      difference among the groups at each time point regarding protein or gene
      expression of MAPRE1. We concluded that internalization of Cx43 into the
      cytoplasm occurred during ischemia, which was partially mediated through
      endocytosis, not by the change of Cx43 quantity. Moreover, internalization was
      not related to microtubule transport.
FAU - Xie, Hongyan
AU  - Xie H
AD  - Department of Neurology, Affiliated Hospital of Taishan Medical University,
      Tai'an 271000, China.
FAU - Cui, Yu
AU  - Cui Y
AD  - Department of Neurosurgery, Affiliated Hospital of Taishan Medical University,
      Tai'an 271000, China.
FAU - Hou, Shuai
AU  - Hou S
AD  - Department of Neurology, The First Hospital of Jilin University, Changchun
      130021, China.
FAU - Wang, Juan
AU  - Wang J
AD  - Department of Neurology, Affiliated Hospital of Taishan Medical University,
      Tai'an 271000, China.
FAU - Miao, Jing
AU  - Miao J
AD  - Department of Neurology, The First Hospital of Jilin University, Changchun
      130021, China.
FAU - Deng, Fang
AU  - Deng F
AUID- ORCID: 0000-0001-7279-9841
AD  - Department of Neurology, The First Hospital of Jilin University, Changchun
      130021, China.
FAU - Feng, Jiachun
AU  - Feng J
AUID- ORCID: 0000-0003-4845-424X
AD  - Department of Neurology, The First Hospital of Jilin University, Changchun
      130021, China.
LA  - eng
PT  - Journal Article
DEP - 20170323
PL  - United States
TA  - Biomed Res Int
JT  - BioMed research international
JID - 101600173
PMC - PMC5382357
EDAT- 2017/04/21 06:00
MHDA- 2017/04/21 06:00
CRDT- 2017/04/21 06:00
PHST- 2016/12/09 [received]
PHST- 2017/02/23 [revised]
PHST- 2017/03/08 [accepted]
AID - 10.1155/2017/5064683 [doi]
PST - ppublish
SO  - Biomed Res Int. 2017;2017:5064683. doi: 10.1155/2017/5064683. Epub 2017 Mar 23.

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