dc.contributor.author |
Görbe, Anikó |
|
dc.contributor.author |
Varga, Zoltán |
|
dc.contributor.author |
Pálóczi, János |
|
dc.contributor.author |
S. Rungarunlert |
|
dc.contributor.author |
N. Klincumhom |
|
dc.contributor.author |
Pirity, Melinda |
|
dc.contributor.author |
R. Madonna |
|
dc.contributor.author |
T. Eschenhagen |
|
dc.contributor.author |
Dinnyés, András |
|
dc.contributor.author |
Csont, Tamás Bálint |
|
dc.contributor.author |
Ferdinandy, Péter |
|
dc.date.accessioned |
2018-08-30T09:16:56Z |
|
dc.date.available |
2018-08-30T09:16:56Z |
|
dc.date.issued |
2014 |
|
dc.identifier |
84896715484 |
|
dc.identifier.citation |
pagination=258-264;
journalVolume=56;
journalIssueNumber=3;
journalTitle=MOLECULAR BIOTECHNOLOGY; |
|
dc.identifier.uri |
http://repo.lib.semmelweis.hu//handle/123456789/6238 |
|
dc.identifier.uri |
doi:10.1007/s12033-013-9704-2 |
|
dc.description.abstract |
Embryonic stem cell (ESC)-derived cardiomyocytes are a promising
cell source for the screening for potential cytoprotective
molecules against ischemia/reperfusion injury, however, little
is known on their behavior in hypoxia/reoxygenation conditions.
Here we tested the cytoprotective effect of the NO-donor SNAP
and its downstream cellular pathway. Mouse ESC-derived
cardiomyocytes were subjected to 150-min simulated ischemia (SI)
followed by 120-min reoxygenation or corresponding non-ischemic
conditions. The following treatments were applied during SI or
normoxia: the NO-donor S-Nitroso-N-acetyl-D,L-penicillamine
(SNAP), the protein kinase G (PKG) inhibitor, the KATP channel
blocker glibenclamide, the particulate guanylate cyclase
activator brain type natriuretic peptide (BNP), and a non-
specific NO synthase inhibitor (N-Nitro-L-arginine, L-NNA) alone
or in different combinations. Viability of cells was assayed by
propidium iodide staining. SNAP attenuated SI-induced cell death
in a concentration-dependent manner, and this protection was
attenuated by inhibition of either PKG or KATP channels.
However, SI-induced cell death was not affected by BNP or by L-
NNA. We conclude that SNAP protects mESC-derived cardiomyocytes
against SI/R injury and that soluble guanylate-cyclase, PKG, and
KATP channels play a role in the downstream pathway of SNAP-
induced cytoprotection. The present mESC-derived cardiomyocyte-
based screening platform is a useful tool for discovery of
cytoprotective molecules. |
|
dc.relation.ispartof |
urn:issn:1073-6085 |
|
dc.title |
Cytoprotection by the NO-donor SNAP against ischemia/reoxygenation injury in mouse embryonic stem cell-derived cardiomyocytes |
|
dc.type |
Journal Article |
|
dc.date.updated |
2018-08-28T20:37:44Z |
|
dc.language.rfc3066 |
en |
|
dc.identifier.mtmt |
2335403 |
|
dc.identifier.wos |
000331721500008 |
|
dc.identifier.pubmed |
24078218 |
|
dc.contributor.department |
SE/AOK/I/Farmakológiai és Farmakoterápiás Intézet |
|
dc.contributor.institution |
Semmelweis Egyetem |
|
dc.mtmt.swordnote |
Görbe A és Varga ZV megosztott első szerző! |
|