PMID- 26303836
OWN - NLM
STAT- MEDLINE
DCOM- 20170731
LR  - 20181113
IS  - 1423-0151 (Electronic)
IS  - 1011-7571 (Print)
IS  - 1011-7571 (Linking)
VI  - 25 Suppl 1
IP  - Suppl 1
DP  - 2016
TI  - The Role of Activated Microglia and Resident Macrophages in the Neurovascular 
      Unit during Cerebral Ischemia: Is the Jury Still Out?
PG  - 3-14
LID - 10.1159/000435858 [doi]
AB  - Paracrine signaling in the neurovascular unit (NVU) is aimed to adjust the supply 
      of oxygen and nutrients to metabolic demands of the brain in a feed-forward 
      manner. Cerebral ischemia (CI) severely disrupts this homeostatic mechanism and 
      also causes activation of microglia and resident macrophages in the brain. 
      Contradictory data exist on the time pattern of microglial activation and 
      polarization during CI, on molecular mechanisms that trigger them and on effects 
      of microglia-derived cytokines on brain cells. It appears that conditions that 
      occur during transient ischemia or in the penumbra of focal ischemia in vivo or 
      equivalent conditions in vitro trigger polarization of resting 
      microglia/macrophages into the M2 phenotype, which mainly exerts 
      anti-inflammatory and protective effects in the brain, while prolonged ischemia 
      with abundant necrosis promotes microglial polarization into the M1 phenotype. 
      During the later stages of recovery, microglia that polarized initially into the 
      M2 phenotype can shift into the M1 phenotype. Thus, it appears that cells with 
      both phenotypes are present in the affected area, but their relative amount 
      changes in time and probably depends on the proximity to the ischemic core. It 
      was assumed that cells with the M1 phenotype exert detrimental effects on neurons 
      and contribute to the blood-brain barrier opening. Several M1 phenotype-specific 
      cytokines exert protective effects on astrocytes, which could be important for 
      reactive gliosis occurring after ischemia. Thus, whether or not suppression of 
      microglial activity after CI is beneficial for neurological outcome still remains 
      unclear and current evidence suggests that no simple answer could be given to 
      this question.
CI  - (c) 2015 S. Karger AG, Basel.
FAU - Barakat, Rawan
AU  - Barakat R
AD  - Department of Physiology, Faculty of Medicine, Kuwait University, Kuwait City, 
      Kuwait.
FAU - Redzic, Zoran
AU  - Redzic Z
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20150819
PL  - Switzerland
TA  - Med Princ Pract
JT  - Medical principles and practice : international journal of the Kuwait University, 
      Health Science Centre
JID - 8901334
SB  - IM
MH  - Brain Ischemia/*metabolism/*pathology
MH  - Humans
MH  - Macrophage Activation/*physiology
MH  - Macrophages/*metabolism
MH  - Microglia/metabolism/*pathology
PMC - PMC5588523
EDAT- 2015/08/26 06:00
MHDA- 2017/08/02 06:00
PMCR- 2015/08/19
CRDT- 2015/08/26 06:00
PHST- 2015/03/15 00:00 [received]
PHST- 2015/06/10 00:00 [accepted]
PHST- 2015/08/26 06:00 [entrez]
PHST- 2015/08/26 06:00 [pubmed]
PHST- 2017/08/02 06:00 [medline]
PHST- 2015/08/19 00:00 [pmc-release]
AID - 000435858 [pii]
AID - mpp-0025-0003 [pii]
AID - 10.1159/000435858 [doi]
PST - ppublish
SO  - Med Princ Pract. 2016;25 Suppl 1(Suppl 1):3-14. doi: 10.1159/000435858. Epub 2015 
      Aug 19.