PMID- 22750211
OWN - NLM
STAT- MEDLINE
DCOM- 20121113
LR  - 20120730
IS  - 1872-7972 (Electronic)
IS  - 0304-3940 (Linking)
VI  - 523
IP  - 2
DP  - 2012 Aug 15
TI  - Effect of PACAP on MAP kinases, Akt and cytokine expressions in rat retinal 
      hypoperfusion.
PG  - 93-8
LID - 10.1016/j.neulet.2012.06.044 [doi]
AB  - Pituitary adenylate cyclase activating polypeptide (PACAP) is known for its 
      potent neuroprotective effects, including the retinoprotective actions in several 
      types of retinal injuries. We have shown earlier that PACAP treatment causes 
      activation of protective pathways and inhibition of pro-apoptotic signaling in 
      excitotoxic retinal lesions. The aim of the present study was to gain insight 
      into the in vivo protective mechanism of PACAP in retinal hypoperfusion injury 
      induced by bilateral common carotid artery occlusion (BCCAO). Rats underwent 
      BCCAO and received intravitreal PACAP (PACAP38) treatment. We investigated the 
      activation level of the protective Akt pathway as well as the different mitogen 
      activated protein kinases (MAPKs) by Western blot analysis and the expression of 
      cytokines using a cytokine array kit. We found that PACAP treatment alone did not 
      influence the phosphorylation of Akt or the MAPKs, but decreased the 
      hypoperfusion-induced activation of both p38MAPK and JNK and increased the 
      activation of the protective Akt and ERK1/2 in hypoperfused retinas. The cytokine 
      profile was dramatically changed after BCCAO, with most cytokines and chemokines 
      showing an increase, which was attenuated by PACAP (such as CINC, CNTF, 
      fractalkine, sICAM, IL-1, LIX, Selectin, MIP-1, RANTES and TIMP-1). In addition, 
      PACAP increased the expression of VEGF and thymus chemokine. The present results 
      provide further insight into the neuroprotective mechanism induced by PACAP in 
      ischemic retinal injuries, showing that PACAP ameliorates hypoperfusion injury 
      involving Akt, MAPK pathways and anti-inflammatory actions.
CI  - Copyright (c) 2012 Elsevier Ireland Ltd. All rights reserved.
FAU - Szabo, Aliz
AU  - Szabo A
AD  - Department of Biochemistry and Medical Chemistry, University of Pecs, Pecs, 
      Hungary.
FAU - Danyadi, Bese
AU  - Danyadi B
FAU - Bognar, Eszter
AU  - Bognar E
FAU - Szabadfi, Krisztina
AU  - Szabadfi K
FAU - Fabian, Eszter
AU  - Fabian E
FAU - Kiss, Peter
AU  - Kiss P
FAU - Mester, Laszlo
AU  - Mester L
FAU - Manavalan, Sridharan
AU  - Manavalan S
FAU - Atlasz, Tamas
AU  - Atlasz T
FAU - Gabriel, Robert
AU  - Gabriel R
FAU - Toth, Gabor
AU  - Toth G
FAU - Tamas, Andrea
AU  - Tamas A
FAU - Reglodi, Dora
AU  - Reglodi D
FAU - Kovacs, Krisztina
AU  - Kovacs K
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20120626
PL  - Ireland
TA  - Neurosci Lett
JT  - Neuroscience letters
JID - 7600130
RN  - 0 (Cytokines)
RN  - 0 (Pituitary Adenylate Cyclase-Activating Polypeptide)
RN  - EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
RN  - EC 2.7.11.24 (Mitogen-Activated Protein Kinases)
SB  - IM
MH  - Animals
MH  - Carotid Artery, Common/physiopathology
MH  - Carotid Stenosis/complications
MH  - Cytokines/*metabolism
MH  - Enzyme Activation
MH  - Ischemia/etiology/*metabolism
MH  - Male
MH  - Mitogen-Activated Protein Kinases/*metabolism
MH  - Pituitary Adenylate Cyclase-Activating Polypeptide/pharmacology/*physiology
MH  - Proto-Oncogene Proteins c-akt/*metabolism
MH  - Rats
MH  - Rats, Wistar
MH  - Retina/drug effects/*metabolism
MH  - Retinal Vessels/drug effects/*physiopathology
MH  - Signal Transduction
EDAT- 2012/07/04 06:00
MHDA- 2012/11/14 06:00
CRDT- 2012/07/04 06:00
PHST- 2012/05/05 00:00 [received]
PHST- 2012/06/15 00:00 [revised]
PHST- 2012/06/17 00:00 [accepted]
PHST- 2012/07/04 06:00 [entrez]
PHST- 2012/07/04 06:00 [pubmed]
PHST- 2012/11/14 06:00 [medline]
AID - S0304-3940(12)00852-X [pii]
AID - 10.1016/j.neulet.2012.06.044 [doi]
PST - ppublish
SO  - Neurosci Lett. 2012 Aug 15;523(2):93-8. doi: 10.1016/j.neulet.2012.06.044. Epub 
      2012 Jun 26.