PMID- 21633713
OWN - NLM
STAT- MEDLINE
DCOM- 20110926
LR  - 20211020
IS  - 1090-0535 (Electronic)
IS  - 1090-0535 (Linking)
VI  - 17
DP  - 2011
TI  - Inhalative preconditioning with hydrogen sulfide attenuated apoptosis after 
      retinal ischemia/reperfusion injury.
PG  - 1275-86
AB  - PURPOSE: Retinal ischemia/reperfusion (I/R) injury plays an important role in the 
      pathophysiology of various ocular diseases. Retinal ganglion cells (RGCs) are 
      particularly vulnerable to ischemia. Hydrogen sulfide (H(2)S) was recently shown 
      to be neuroprotective in the brain and retina due to its antiapoptotic effects. 
      Rapid preconditioning of retinal neurons by inhaled H(2)S before I/R injury may 
      reduce apoptosis in the rat retina. METHODS: I/R injury was created on the left 
      eye of rats (n=8) with or without inhaled H(2)S preconditioning (80 ppm) for one 
      hour before ischemia. Densities of fluorogold prelabeled RGCs were analyzed 7 
      days after injury in retinal whole mounts. Retinal tissue was harvested to 
      analyze protein expression of heat shock protein (HSP)-90 and the 
      mitogen-activated protein kinases (MAPKs) c-jun N-terminal kinase (JNK), 
      extracellular signal-regulated kinase (ERK)1/2 and p38 to elucidate a possible 
      pathway of neuroprotection. DNA binding activity of the transcription factors 
      nuclear factor-kappa-light-chain-enhancer of activated B-cells (NF-kappaB), cyclic 
      adenosine monophosphate response element binding protein (CREB), and heat shock 
      element (HSE), as well as caspase-3 cleavage and activity, were determined. 
      Retinal sections were further assessed using anti-glial fibrillary acidic protein 
      staining. RESULTS: RGC death after I/R injury decreased by 41.5% after H(2)S 
      preconditioning compared to room air (p<0.001). H(2)S inhalation before ischemia 
      reduced caspase-3 cleavage (p<0.001) and attenuated caspase-3 activity (p<0.001). 
      Furthermore, HSP-90 expression was significantly elevated in the retina after 
      H(2)S preconditioning. NF-kappaB but not CREB or HSE showed specific, H2S-dependent 
      regulation, as well as the MAPKs ERK1/2 and JNK but not p38. CONCLUSIONS: H(2)S 
      preconditioning mediates antiapoptotic effects in retinal I/R injury, thus 
      exhibiting neuroprotection. Based on these observations, H(2)S could represent a 
      novel and promising therapeutic agent to counteract neuronal injuries in the eye. 
      Further studies are needed to prove H(2)S's neuroprotective propensity using a 
      postconditioning approach.
CI  - (c) 2011 Molecular Vision
FAU - Biermann, Julia
AU  - Biermann J
AD  - University Eye Hospital Freiburg, Freiburg, Germany. 
      julia.biermann@uniklinik-freiburg.de
FAU - Lagreze, Wolf A
AU  - Lagreze WA
FAU - Schallner, Nils
AU  - Schallner N
FAU - Schwer, Christian I
AU  - Schwer CI
FAU - Goebel, Ulrich
AU  - Goebel U
LA  - eng
PT  - Journal Article
DEP - 20110507
PL  - United States
TA  - Mol Vis
JT  - Molecular vision
JID - 9605351
RN  - 0 (Caspase Inhibitors)
RN  - 0 (Glial Fibrillary Acidic Protein)
RN  - 0 (HSP90 Heat-Shock Proteins)
RN  - 0 (NF-kappa B)
RN  - 0 (Neuroprotective Agents)
RN  - 9007-49-2 (DNA)
RN  - EC 2.7.11.24 (Mitogen-Activated Protein Kinases)
RN  - YY9FVM7NSN (Hydrogen Sulfide)
SB  - IM
MH  - Administration, Inhalation
MH  - Animals
MH  - Apoptosis/*drug effects
MH  - Caspase Inhibitors
MH  - Cell Death/drug effects
MH  - DNA/metabolism
MH  - Female
MH  - Glial Fibrillary Acidic Protein/metabolism
MH  - HSP90 Heat-Shock Proteins/metabolism
MH  - Hydrogen Sulfide/*administration & dosage
MH  - Ischemic Preconditioning/*methods
MH  - Male
MH  - Mitogen-Activated Protein Kinases/metabolism
MH  - NF-kappa B/metabolism
MH  - Neuroprotective Agents/*administration & dosage
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Reperfusion Injury/pathology/*physiopathology
MH  - Retina/metabolism
MH  - Retinal Ganglion Cells/drug effects
MH  - Retinal Vessels/drug effects/*physiopathology
MH  - Time Factors
MH  - Tissue Distribution
PMC - PMC3103742
EDAT- 2011/06/03 06:00
MHDA- 2011/09/29 06:00
PMCR- 2011/01/01
CRDT- 2011/06/03 06:00
PHST- 2010/10/22 00:00 [received]
PHST- 2011/05/03 00:00 [accepted]
PHST- 2011/06/03 06:00 [entrez]
PHST- 2011/06/03 06:00 [pubmed]
PHST- 2011/09/29 06:00 [medline]
PHST- 2011/01/01 00:00 [pmc-release]
AID - 143 [pii]
AID - 2010MOLVIS0458 [pii]
PST - ppublish
SO  - Mol Vis. 2011;17:1275-86. Epub 2011 May 7.