PMID- 23601050
OWN - NLM
STAT- MEDLINE
DCOM- 20140219
LR  - 20130729
IS  - 1440-1681 (Electronic)
IS  - 0305-1870 (Linking)
VI  - 40
IP  - 8
DP  - 2013 Aug
TI  - Brain and retinal microglia in health and disease: an unrecognized target of the 
      renin-angiotensin system.
PG  - 571-9
LID - 10.1111/1440-1681.12099 [doi]
AB  - Microglia are the resident immune cells within the brain and retina, commonly 
      known as the macrophages of the central nervous system (CNS). Microglia survey 
      the surrounding milieu to eliminate invading microbes, clear cellular debris and 
      enforce programmed cell death by removing apoptotic cells. Complementary to their 
      'house-keeping' role, microglia are capable of releasing brain-derived 
      neurotrophic factor (BDNF), as well as various anti-inflammatory cytokines that 
      sustain and support neuronal survival. Although microglia are essential for 
      maintaining a healthy CNS, paradoxically they may undergo phenotypic changes to 
      influence numerous neurodegenerative disorders, including Parkinson's disease and 
      Alzheimer's disease. Understanding the underlying mechanisms that determine 
      whether microglia are supportive or toxic could elucidate novel and more 
      effective therapeutic targets to treat an array of neurological and retinal 
      diseases. Although relatively little is known about the influences that evoke 
      phenotypic changes in the microglial population, there is accumulating evidence 
      illustrating an interaction with the renin-angiotensin system (RAS). The 
      angiotensin AT1 and AT2 receptors may have differential roles in mediating the 
      activity of microglia. Understanding the actions of these angiotensin receptors 
      will be important in defining whether microglia are an important therapeutic 
      target for RAS blockade in brain and ocular diseases.
CI  - (c) 2013 Wiley Publishing Asia Pty Ltd.
FAU - McCarthy, Claudia A
AU  - McCarthy CA
AD  - Department of Pharmacology, Monash University, Clayton, Alfred Medical Research 
      and Education Precinct, Melbourne, Victoria, Australia.
FAU - Widdop, Robert E
AU  - Widdop RE
FAU - Deliyanti, Devy
AU  - Deliyanti D
FAU - Wilkinson-Berka, Jennifer L
AU  - Wilkinson-Berka JL
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
PL  - Australia
TA  - Clin Exp Pharmacol Physiol
JT  - Clinical and experimental pharmacology & physiology
JID - 0425076
SB  - IM
MH  - Animals
MH  - Brain/*cytology
MH  - Gene Expression Regulation/physiology
MH  - Microglia/*cytology/*physiology
MH  - Renin-Angiotensin System/*physiology
MH  - Retina/*cytology
OTO - NOTNLM
OT  - angiotensin
OT  - angiotensin AT2 receptor
OT  - brain
OT  - microglia
OT  - retina
EDAT- 2013/04/23 06:00
MHDA- 2014/02/20 06:00
CRDT- 2013/04/23 06:00
PHST- 2012/12/21 00:00 [received]
PHST- 2013/04/12 00:00 [revised]
PHST- 2013/04/15 00:00 [accepted]
PHST- 2013/04/23 06:00 [entrez]
PHST- 2013/04/23 06:00 [pubmed]
PHST- 2014/02/20 06:00 [medline]
AID - 10.1111/1440-1681.12099 [doi]
PST - ppublish
SO  - Clin Exp Pharmacol Physiol. 2013 Aug;40(8):571-9. doi: 10.1111/1440-1681.12099.