schliessen

Filtern

 

Bibliotheken

Protection by Nitric Oxide Donors of Isolated Rat Hearts Is Associated with Activation of Redox Metabolism and Ferritin Accumulation.

Preconditioning (PC) procedures (ischemic or pharmacological) are powerful procedures used for attaining protection against prolonged ischemia and reperfusion (I/R) injury, in a variety of organs, including the heart. The detailed molecular mechanisms underlying the protection by PC are however, com... Full description

Journal Title: PloS one 2016, Vol.11(7), p.e0159951
Main Author: Grievink, Hilbert
Other Authors: Zeltcer, Galina , Drenger, Benjamin , Berenshtein, Eduard , Chevion, Mordechai
Format: Electronic Article Electronic Article
Language: English
Subjects:
ID: E-ISSN: 1932-6203 ; DOI: 1932-6203 ; DOI: 10.1371/journal.pone.0159951
Link: http://search.proquest.com/docview/1807278966/?pq-origsite=primo
Zum Text:
SendSend as email Add to Book BagAdd to Book Bag
Staff View
recordid: proquest1807278966
title: Protection by Nitric Oxide Donors of Isolated Rat Hearts Is Associated with Activation of Redox Metabolism and Ferritin Accumulation.
format: Article
creator:
  • Grievink, Hilbert
  • Zeltcer, Galina
  • Drenger, Benjamin
  • Berenshtein, Eduard
  • Chevion, Mordechai
subjects:
  • Aconitate Hydratase–Metabolism
  • Animals–Metabolism
  • Cytosol–Metabolism
  • Ferritins–Drug Effects
  • Heart–Drug Effects
  • Hemodynamics–Metabolism
  • Iron–Metabolism
  • Ischemic Preconditioning, Myocardial–Metabolism
  • Male–Metabolism
  • Methionine–Pathology
  • Methionine Sulfoxide Reductases–Physiopathology
  • Myocardial Reperfusion Injury–Metabolism
  • Myocardium–Pharmacology
  • Nitric Oxide Donors–Drug Effects
  • Oxidation-Reduction–Pharmacology
  • Protective Agents–Pharmacology
  • Rats–Pharmacology
  • Nitric Oxide Donors
  • Protective Agents
  • Ferritins
  • Methionine
  • Iron
  • Methionine Sulfoxide Reductases
  • Methionine Sulfoxide Reductase
  • Aconitate Hydratase
ispartof: PloS one, 2016, Vol.11(7), p.e0159951
description: Preconditioning (PC) procedures (ischemic or pharmacological) are powerful procedures used for attaining protection against prolonged ischemia and reperfusion (I/R) injury, in a variety of organs, including the heart. The detailed molecular mechanisms underlying the protection by PC are however, complex and only partially understood. Recently, an 'iron-based mechanism' (IBM), that includes de novo ferritin synthesis and accumulation, was proposed to explain the specific steps in cardioprotection generated by IPC. The current study investigated whether nitric oxide (NO), generated by exogenous NO-donors, could play a role in the observed IBM of cardioprotection by IPC. Therefore, three distinct NO-donors were investigated at different concentrations (1-10 [mu]M): sodium nitroprusside (SNP), 3-morpholinosydnonimine (SIN-1) and S-nitroso-N-acetylpenicillamine (SNAP). Isolated rat hearts were retrogradely perfused using the Langendorff configuration and subjected to prolonged ischemia and reperfusion with or without pretreatment by NO-donors. Hemodynamic parameters, infarct sizes and proteins of the methionine-centered redox cycle (MCRC) were analyzed, as well as cytosolic aconitase (CA) activity and ferritin protein levels. All NO-donors had significant effects on proteins involved in the MCRC system. Nonetheless, pretreatment with 10 [mu]M SNAP was found to evoke the strongest effects on Msr activity, thioredoxin and thioredoxin reductase protein levels. These effects were accompanied with a significant reduction in infarct size, increased CA activity, and ferritin accumulation. Conversely, pretreatment with 2 [mu]M SIN-1 increased infarct size and was associated with slightly lower ferritin protein levels. In conclusion, the abovementioned findings indicate that NO, depending on its bio-active redox form, can regulate iron metabolism and plays a role in the IBM of cardioprotection against reperfusion injury.
language: eng
source:
identifier: E-ISSN: 1932-6203 ; DOI: 1932-6203 ; DOI: 10.1371/journal.pone.0159951
fulltext: fulltext
issn:
  • 19326203
  • 1932-6203
url: Link


@attributes
ID999541934
RANK0.07
NO1
SEARCH_ENGINEprimo_central_multiple_fe
SEARCH_ENGINE_TYPEPrimo Central Search Engine
LOCALfalse
PrimoNMBib
record
control
sourcerecordid1807278966
sourceidproquest
recordidTN_proquest1807278966
sourcesystemOther
pqid1807278966
galeid459060950
display
typearticle
titleProtection by Nitric Oxide Donors of Isolated Rat Hearts Is Associated with Activation of Redox Metabolism and Ferritin Accumulation.
creatorGrievink, Hilbert ; Zeltcer, Galina ; Drenger, Benjamin ; Berenshtein, Eduard ; Chevion, Mordechai
contributorGrievink, Hilbert (correspondence author) ; Grievink, Hilbert (record owner)
ispartofPloS one, 2016, Vol.11(7), p.e0159951
identifier
subjectAconitate Hydratase–Metabolism ; Animals–Metabolism ; Cytosol–Metabolism ; Ferritins–Drug Effects ; Heart–Drug Effects ; Hemodynamics–Metabolism ; Iron–Metabolism ; Ischemic Preconditioning, Myocardial–Metabolism ; Male–Metabolism ; Methionine–Pathology ; Methionine Sulfoxide Reductases–Physiopathology ; Myocardial Reperfusion Injury–Metabolism ; Myocardium–Pharmacology ; Nitric Oxide Donors–Drug Effects ; Oxidation-Reduction–Pharmacology ; Protective Agents–Pharmacology ; Rats–Pharmacology ; Nitric Oxide Donors ; Protective Agents ; Ferritins ; Methionine ; Iron ; Methionine Sulfoxide Reductases ; Methionine Sulfoxide Reductase ; Aconitate Hydratase
languageeng
source
descriptionPreconditioning (PC) procedures (ischemic or pharmacological) are powerful procedures used for attaining protection against prolonged ischemia and reperfusion (I/R) injury, in a variety of organs, including the heart. The detailed molecular mechanisms underlying the protection by PC are however, complex and only partially understood. Recently, an 'iron-based mechanism' (IBM), that includes de novo ferritin synthesis and accumulation, was proposed to explain the specific steps in cardioprotection generated by IPC. The current study investigated whether nitric oxide (NO), generated by exogenous NO-donors, could play a role in the observed IBM of cardioprotection by IPC. Therefore, three distinct NO-donors were investigated at different concentrations (1-10 [mu]M): sodium nitroprusside (SNP), 3-morpholinosydnonimine (SIN-1) and S-nitroso-N-acetylpenicillamine (SNAP). Isolated rat hearts were retrogradely perfused using the Langendorff configuration and subjected to prolonged ischemia and reperfusion with or without pretreatment by NO-donors. Hemodynamic parameters, infarct sizes and proteins of the methionine-centered redox cycle (MCRC) were analyzed, as well as cytosolic aconitase (CA) activity and ferritin protein levels. All NO-donors had significant effects on proteins involved in the MCRC system. Nonetheless, pretreatment with 10 [mu]M SNAP was found to evoke the strongest effects on Msr activity, thioredoxin and thioredoxin reductase protein levels. These effects were accompanied with a significant reduction in infarct size, increased CA activity, and ferritin accumulation. Conversely, pretreatment with 2 [mu]M SIN-1 increased infarct size and was associated with slightly lower ferritin protein levels. In conclusion, the abovementioned findings indicate that NO, depending on its bio-active redox form, can regulate iron metabolism and plays a role in the IBM of cardioprotection against reperfusion injury.
version9
lds50peer_reviewed
links
openurl$$Topenurl_article
openurlfulltext$$Topenurlfull_article
backlink$$Uhttp://search.proquest.com/docview/1807278966/?pq-origsite=primo$$EView_record_in_ProQuest_(subscribers_only)
search
creatorcontrib
0Grievink, Hilbert
1Zeltcer, Galina
2Drenger, Benjamin
3Berenshtein, Eduard
4Chevion, Mordechai
titleProtection by Nitric Oxide Donors of Isolated Rat Hearts Is Associated with Activation of Redox Metabolism and Ferritin Accumulation.
subject
0Aconitate Hydratase–Metabolism
1Animals–Metabolism
2Cytosol–Metabolism
3Ferritins–Drug Effects
4Heart–Drug Effects
5Hemodynamics–Metabolism
6Iron–Metabolism
7Ischemic Preconditioning, Myocardial–Metabolism
8Male–Metabolism
9Methionine–Pathology
10Methionine Sulfoxide Reductases–Physiopathology
11Myocardial Reperfusion Injury–Metabolism
12Myocardium–Pharmacology
13Nitric Oxide Donors–Drug Effects
14Oxidation-Reduction–Pharmacology
15Protective Agents–Pharmacology
16Rats–Pharmacology
17Nitric Oxide Donors
18Protective Agents
19Ferritins
20Methionine
21Iron
22Methionine Sulfoxide Reductases
23Methionine Sulfoxide Reductase
24Aconitate Hydratase
general
0English
11932-6203
210.1371/journal.pone.0159951
3MEDLINE (ProQuest)
4ProQuest Biological Science Collection
5ProQuest Natural Science Collection
6ProQuest SciTech Collection
7Biological Science Database
8Natural Science Collection
9SciTech Premium Collection
10Health Research Premium Collection
11Health Research Premium Collection (Alumni edition)
sourceidproquest
recordidproquest1807278966
issn
019326203
11932-6203
rsrctypearticle
creationdate2016
addtitlePloS one
searchscope
01007527
11007944
210000004
310000038
410000050
510000120
610000159
710000238
810000253
910000260
1010000270
1110000271
1210000302
13proquest
scope
01007527
11007944
210000004
310000038
410000050
510000120
610000159
710000238
810000253
910000260
1010000270
1110000271
1210000302
13proquest
lsr43
01007527false
11007944false
210000004false
310000038false
410000050false
510000120false
610000159false
710000238false
810000253false
910000260false
1010000270false
1110000271false
1210000302false
contributorGrievink, Hilbert
startdate20160101
enddate20160101
citationpf e0159951 pt e0159951 vol 11 issue 7
lsr30VSR-Enriched:[description, galeid, pqid]
sort
titleProtection by Nitric Oxide Donors of Isolated Rat Hearts Is Associated with Activation of Redox Metabolism and Ferritin Accumulation.
authorGrievink, Hilbert ; Zeltcer, Galina ; Drenger, Benjamin ; Berenshtein, Eduard ; Chevion, Mordechai
creationdate20160101
lso0120160101
facets
frbrgroupid1504313262937968526
frbrtype5
newrecords20181218
languageeng
creationdate2016
topic
0Aconitate Hydratase–Metabolism
1Animals–Metabolism
2Cytosol–Metabolism
3Ferritins–Drug Effects
4Heart–Drug Effects
5Hemodynamics–Metabolism
6Iron–Metabolism
7Ischemic Preconditioning, Myocardial–Metabolism
8Male–Metabolism
9Methionine–Pathology
10Methionine Sulfoxide Reductases–Physiopathology
11Myocardial Reperfusion Injury–Metabolism
12Myocardium–Pharmacology
13Nitric Oxide Donors–Drug Effects
14Oxidation-Reduction–Pharmacology
15Protective Agents–Pharmacology
16Rats–Pharmacology
17Nitric Oxide Donors
18Protective Agents
19Ferritins
20Methionine
21Iron
22Methionine Sulfoxide Reductases
23Methionine Sulfoxide Reductase
24Aconitate Hydratase
collection
0MEDLINE (ProQuest)
1ProQuest Biological Science Collection
2ProQuest Natural Science Collection
3ProQuest SciTech Collection
4Biological Science Database
5Natural Science Collection
6SciTech Premium Collection
7Health Research Premium Collection
8Health Research Premium Collection (Alumni edition)
prefilterarticles
rsrctypearticles
creatorcontrib
0Grievink, Hilbert
1Zeltcer, Galina
2Drenger, Benjamin
3Berenshtein, Eduard
4Chevion, Mordechai
jtitlePloS one
toplevelpeer_reviewed
delivery
delcategoryRemote Search Resource
fulltextfulltext
addata
aulast
0Grievink
1Zeltcer
2Drenger
3Berenshtein
4Chevion
aufirst
0Hilbert
1Galina
2Benjamin
3Eduard
4Mordechai
au
0Grievink, Hilbert
1Zeltcer, Galina
2Drenger, Benjamin
3Berenshtein, Eduard
4Chevion, Mordechai
addauGrievink, Hilbert
atitleProtection by Nitric Oxide Donors of Isolated Rat Hearts Is Associated with Activation of Redox Metabolism and Ferritin Accumulation.
jtitlePloS one
risdate20160101
volume11
issue7
spagee0159951
epagee0159951
pagese0159951
eissn1932-6203
formatjournal
genrearticle
ristypeJOUR
doi10.1371/journal.pone.0159951
urlhttp://search.proquest.com/docview/1807278966/
date2016-01-01