PMID- 27619151
OWN - NLM
STAT- MEDLINE
DCOM- 20170605
LR  - 20231213
IS  - 1474-9726 (Electronic)
IS  - 1474-9718 (Print)
IS  - 1474-9718 (Linking)
VI  - 16
IP  - 1
DP  - 2017 Feb
TI  - Caloric restriction increases brain mitochondrial calcium retention capacity and 
      protects against excitotoxicity.
PG  - 73-81
LID - 10.1111/acel.12527 [doi]
AB  - Caloric restriction (CR) protects against many cerebral pathological conditions 
      that are associated with excitotoxic damage and calcium overload, although the 
      mechanisms are still poorly understood. Here we show that CR strongly protects 
      against excitotoxic insults in vitro and in vivo in a manner associated with 
      significant changes in mitochondrial function. CR increases electron transport 
      chain activity, enhances antioxidant defenses, and favors mitochondrial calcium 
      retention capacity in the brain. These changes are accompanied by a decrease in 
      cyclophilin D activity and acetylation and an increase in Sirt3 expression. This 
      suggests that Sirt3-mediated deacetylation and inhibition of cyclophilin D in CR 
      promote the inhibition of mitochondrial permeability transition, resulting in 
      enhanced mitochondrial calcium retention. Altogether, our results indicate that 
      enhanced mitochondrial calcium retention capacity underlies the beneficial 
      effects of CR against excitotoxic conditions. This protection may explain the 
      many beneficial effects of CR in the aging brain.
CI  - (c) 2016 The Authors. Aging Cell published by the Anatomical Society and John Wiley 
      & Sons Ltd.
FAU - Amigo, Ignacio
AU  - Amigo I
AD  - Departamento de Bioquimica, Instituto de Quimica, Universidade de Sao Paulo, Sao 
      Paulo, Brazil.
FAU - Menezes-Filho, Sergio Luiz
AU  - Menezes-Filho SL
AD  - Departamento de Bioquimica, Instituto de Quimica, Universidade de Sao Paulo, Sao 
      Paulo, Brazil.
FAU - Luevano-Martinez, Luis Alberto
AU  - Luevano-Martinez LA
AD  - Departamento de Bioquimica, Instituto de Quimica, Universidade de Sao Paulo, Sao 
      Paulo, Brazil.
FAU - Chausse, Bruno
AU  - Chausse B
AD  - Departamento de Bioquimica, Instituto de Quimica, Universidade de Sao Paulo, Sao 
      Paulo, Brazil.
FAU - Kowaltowski, Alicia J
AU  - Kowaltowski AJ
AD  - Departamento de Bioquimica, Instituto de Quimica, Universidade de Sao Paulo, Sao 
      Paulo, Brazil.
LA  - eng
PT  - Journal Article
DEP - 20160913
PL  - England
TA  - Aging Cell
JT  - Aging cell
JID - 101130839
RN  - 0 (Antioxidants)
RN  - 0 (Peptidyl-Prolyl Isomerase F)
RN  - 0 (Neuroprotective Agents)
RN  - 0 (Neurotoxins)
RN  - 0 (PPIF protein, mouse)
RN  - 3KX376GY7L (Glutamic Acid)
RN  - EC 5.2.1.- (Cyclophilins)
RN  - SY7Q814VUP (Calcium)
SB  - IM
MH  - Acetylation/drug effects
MH  - Animals
MH  - Antioxidants/pharmacology
MH  - Brain/drug effects/metabolism
MH  - Calcium/*metabolism
MH  - *Caloric Restriction
MH  - Cell Death/drug effects
MH  - Peptidyl-Prolyl Isomerase F
MH  - Cyclophilins/metabolism
MH  - Electron Transport/drug effects
MH  - Glutamic Acid/toxicity
MH  - Male
MH  - Mice
MH  - Mitochondria/*metabolism
MH  - Neuroprotective Agents/*metabolism
MH  - Neurotoxins/*toxicity
MH  - Rats, Sprague-Dawley
MH  - Serum/metabolism
PMC - PMC5242290
OTO - NOTNLM
OT  - aging
OT  - brain
OT  - calcium
OT  - caloric restriction
OT  - mitochondria
EDAT- 2016/09/14 06:00
MHDA- 2017/06/06 06:00
PMCR- 2017/02/01
CRDT- 2016/09/14 06:00
PHST- 2016/08/11 00:00 [accepted]
PHST- 2016/09/14 06:00 [pubmed]
PHST- 2017/06/06 06:00 [medline]
PHST- 2016/09/14 06:00 [entrez]
PHST- 2017/02/01 00:00 [pmc-release]
AID - ACEL12527 [pii]
AID - 10.1111/acel.12527 [doi]
PST - ppublish
SO  - Aging Cell. 2017 Feb;16(1):73-81. doi: 10.1111/acel.12527. Epub 2016 Sep 13.