PMID- 25173074
OWN - NLM
STAT- MEDLINE
DCOM- 20150602
LR  - 20141007
IS  - 1872-6240 (Electronic)
IS  - 0006-8993 (Linking)
VI  - 1585
DP  - 2014 Oct 17
TI  - Autophagy and ER-stress contribute to photoreceptor degeneration in cultured 
      adult porcine retina.
PG  - 167-83
LID - S0006-8993(14)01131-7 [pii]
LID - 10.1016/j.brainres.2014.08.055 [doi]
AB  - The aim of this study was to investigate rod and cone photoreceptor degeneration 
      in organotypic cultures of adult porcine retina. Our hypothesis was that the 
      photoreceptors accumulate opsins, which, together with exposure to cyclic dim 
      light illumination, induce autophagy and endoplasmic reticulum stress (ER-stress) 
      to overcome damaging protein overload. For this purpose, retinas were cultured 
      for 48 h and 72 h during which they were illuminated with dim light for 8h/day; 
      specimens were analyzed by means of immunohistochemistry, Western blot, real-time 
      polymerase chain reaction (PCR) and transmission electron microscopy. ER-stress 
      and photoreceptor degeneration was observed in conventionally cultured retinas. 
      The additional stress in the form of dim light illumination for 8h/day resulted 
      in increased levels of the ER-stress markers GRP78/BiP and CHOP, as well as 
      increased level of active caspase-12. Increased autophagic processes in cone and 
      rod photoreceptors were detected by LC3B-II increases and occurrence of 
      autophagosomes at the ultrastructural level. Illumination also resulted in 
      altered protein expression for autophagy inducers such as p62 and Beclin-1. 
      Moreover, there was a decrease in phosphorylated mammalian target of rapamycin 
      (mTOR), which further indicate an increase of autophagy. Rod and cone 
      photoreceptors in retinas from a diurnal animal that were exposed to dim light 
      illumination in vitro displayed autophagy and ER-stress processes. As no 
      alteration of rhodopsin mRNA was observed, autophagy and ER-stress are suggested 
      to decrease rhodopsin protein at the posttranscriptional level.
CI  - Copyright (c) 2014 Elsevier B.V. All rights reserved.
FAU - Mohlin, Camilla
AU  - Mohlin C
AD  - Department of Medicine and Optometry, Linnaeus University, Kalmar, Sweden.
FAU - Taylor, Linnea
AU  - Taylor L
AD  - Department of Ophthalmology, Lund University Hospital, Lund, Sweden.
FAU - Ghosh, Fredrik
AU  - Ghosh F
AD  - Department of Ophthalmology, Lund University Hospital, Lund, Sweden.
FAU - Johansson, Kjell
AU  - Johansson K
AD  - Department of Medicine and Optometry, Linnaeus University, Kalmar, Sweden; School 
      of Health and Medicine, Orebro University, Orebro, Sweden. Electronic address: 
      kjell.johansson@oru.se.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20140828
PL  - Netherlands
TA  - Brain Res
JT  - Brain research
JID - 0045503
RN  - 9009-81-8 (Rhodopsin)
SB  - IM
MH  - Animals
MH  - *Autophagy
MH  - Circadian Rhythm
MH  - *Endoplasmic Reticulum Stress
MH  - Organ Culture Techniques
MH  - Photic Stimulation
MH  - Retinal Cone Photoreceptor Cells/*metabolism/pathology
MH  - Retinal Rod Photoreceptor Cells/*metabolism/pathology
MH  - Rhodopsin/*metabolism
MH  - Swine
MH  - Synapses/ultrastructure
OTO - NOTNLM
OT  - Apoptosis
OT  - Autophagy
OT  - Endoplasmic reticulum stress
OT  - Photoreceptor
OT  - Porcine retina
OT  - Retinal degeneration
EDAT- 2014/09/01 06:00
MHDA- 2015/06/03 06:00
CRDT- 2014/09/01 06:00
PHST- 2014/03/18 00:00 [received]
PHST- 2014/07/23 00:00 [revised]
PHST- 2014/08/12 00:00 [accepted]
PHST- 2014/09/01 06:00 [entrez]
PHST- 2014/09/01 06:00 [pubmed]
PHST- 2015/06/03 06:00 [medline]
AID - S0006-8993(14)01131-7 [pii]
AID - 10.1016/j.brainres.2014.08.055 [doi]
PST - ppublish
SO  - Brain Res. 2014 Oct 17;1585:167-83. doi: 10.1016/j.brainres.2014.08.055. Epub 
      2014 Aug 28.