PMID- 31145968
OWN - NLM
STAT- MEDLINE
DCOM- 20200601
LR  - 20200601
IS  - 1872-9754 (Electronic)
IS  - 0197-0186 (Linking)
VI  - 129
DP  - 2019 Oct
TI  - Role of bone marrow-derived macrophages (BMDMs) in neurovascular interactions 
      during stroke.
PG  - 104480
LID - S0197-0186(19)30114-7 [pii]
LID - 10.1016/j.neuint.2019.104480 [doi]
AB  - Stroke is a leading cause of disability worldwide and hence remains a major 
      medical concern. Besides several pathological features, such as excitotoxicity, 
      peri-infarct depolarization, acidosis, reactive oxygen species generation, 
      apoptosis, and necrosis, dysregulation of the immune system severely affects 
      stroke outcomes. After stroke onset, microglia - the brain-resident macrophage 
      immune cells - and peripheral immune cells affect stoke injury/recovery by 
      releasing pro-inflammatory and/or anti-inflammatory cytokines depending on their 
      microenvironment. These pro- or anti-inflammatory cytokines further affect 
      integrity of the blood brain barrier (BBB) and modulate immune infiltration after 
      stroke. Among peripheral immune cells, bone marrow-derived macrophages (BMDMs) 
      play a critical role in stroke pathology which peaks between three and seven days 
      post-stroke. BMDMs have been extensively studied for their role in exacerbation 
      of stroke injury, however they have rarely been studied for their role in tissue 
      repair. Nonetheless, these reparative roles are gaining attention since recent 
      studies have shown either failure or worsening of long-term post-stroke recovery 
      after blockade of peripheral immune infiltration. These diverse but paradoxical 
      effects of infiltrating monocytes/macrophages encouraged us to summarize the 
      latest findings in neuro-immune and immune-vascular interactions. This review 
      highlights the multifaceted role of BMDMs in stroke onset and resolution, and 
      emphasizes the significance of tapping the potential of these cells to gain 
      better insight into disease progression and therapy.
CI  - Copyright (c) 2019 Elsevier Ltd. All rights reserved.
FAU - Srivastava, Akriti
AU  - Srivastava A
AD  - Department of Neuroscience, UConn Health, Farmington, CT, 06032, USA.
FAU - Srivastava, Pranay
AU  - Srivastava P
AD  - Department of Neuroscience, UConn Health, Farmington, CT, 06032, USA.
FAU - Verma, Rajkumar
AU  - Verma R
AD  - Department of Neuroscience, UConn Health, Farmington, CT, 06032, USA. Electronic 
      address: raverma@uchc.edu.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
DEP - 20190527
PL  - England
TA  - Neurochem Int
JT  - Neurochemistry international
JID - 8006959
RN  - 0 (Cytokines)
SB  - IM
MH  - Blood-Brain Barrier/drug effects/metabolism
MH  - Cytokines/metabolism
MH  - Humans
MH  - Inflammation/*drug therapy/pathology
MH  - Macrophages/*drug effects
MH  - Microglia/*drug effects/metabolism
MH  - Stroke/*drug therapy/pathology
EDAT- 2019/05/31 06:00
MHDA- 2020/06/02 06:00
CRDT- 2019/05/31 06:00
PHST- 2019/03/08 00:00 [received]
PHST- 2019/05/24 00:00 [revised]
PHST- 2019/05/27 00:00 [accepted]
PHST- 2019/05/31 06:00 [pubmed]
PHST- 2020/06/02 06:00 [medline]
PHST- 2019/05/31 06:00 [entrez]
AID - S0197-0186(19)30114-7 [pii]
AID - 10.1016/j.neuint.2019.104480 [doi]
PST - ppublish
SO  - Neurochem Int. 2019 Oct;129:104480. doi: 10.1016/j.neuint.2019.104480. Epub 2019 
      May 27.