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Statements

Subject Item
n2:RIV%2F00216208%3A11310%2F13%3A10189222%21RIV14-MSM-11310___
rdf:type
skos:Concept n13:Vysledek
rdfs:seeAlso
http://dx.doi.org/10.1016/j.exer.2013.10.002
dcterms:description
The purpose of this study was to investigate whether rabbit bone marrow-derived mesenchymal stem cells (MSCs) effectively decrease alkali-induced oxidative stress in the rabbit cornea. The alkali (0.15 N NaOH) was applied on the corneas of the right eyes and then rinsed with tap water. In the first group of rabbits the injured corneas remained untreated. In the second group MSCs were applied on the injured corneal surface immediately after the injury and eyelids sutured for two days. Then the sutures were removed. In the third group nanofiber scaffolds seeded with MSCs (and in the fourth group nanofibers alone) were transferred onto the corneas immediately after the injury and the eyelids sutured. Two days later the eyelid sutures were removed together with the nanofiber scaffolds. The rabbits were sacrificed on days four, ten or fifteen after the injury, and the corneas were examined immunohistochemically, morphologically, for the central corneal thickness (taken as an index of corneal hydration) using an ultrasonic pachymeter and by real-time PCR. Results show that in untreated injured corneas the expression of malondialdehyde (MDA) and nitrotyrosine (NT) (important markers of lipid peroxidation and oxidative stress) appeared in the epithelium. The antioxidant aldehyde dehydrogenase 3A1 (ALDH3A1) decreased in the corneal epithelium, particularly in superficial parts, where apoptotic cell death (detected by active caspase-3) was high. (In control corneal epithelium MDA and NT are absent and ALDH3A1 highly present in all layers of the epithelium. Cell apoptosis are sporadic). In injured untreated cornea further corneal disturbances developed: The expressions of matrix metalloproteinase 9 (MMP9) and proinflammatory cytokines, were high. At the end of experiment (on day 15) the injured untreated corneas were vascularized and numerous inflammatory cells were present in the corneal stroma. The purpose of this study was to investigate whether rabbit bone marrow-derived mesenchymal stem cells (MSCs) effectively decrease alkali-induced oxidative stress in the rabbit cornea. The alkali (0.15 N NaOH) was applied on the corneas of the right eyes and then rinsed with tap water. In the first group of rabbits the injured corneas remained untreated. In the second group MSCs were applied on the injured corneal surface immediately after the injury and eyelids sutured for two days. Then the sutures were removed. In the third group nanofiber scaffolds seeded with MSCs (and in the fourth group nanofibers alone) were transferred onto the corneas immediately after the injury and the eyelids sutured. Two days later the eyelid sutures were removed together with the nanofiber scaffolds. The rabbits were sacrificed on days four, ten or fifteen after the injury, and the corneas were examined immunohistochemically, morphologically, for the central corneal thickness (taken as an index of corneal hydration) using an ultrasonic pachymeter and by real-time PCR. Results show that in untreated injured corneas the expression of malondialdehyde (MDA) and nitrotyrosine (NT) (important markers of lipid peroxidation and oxidative stress) appeared in the epithelium. The antioxidant aldehyde dehydrogenase 3A1 (ALDH3A1) decreased in the corneal epithelium, particularly in superficial parts, where apoptotic cell death (detected by active caspase-3) was high. (In control corneal epithelium MDA and NT are absent and ALDH3A1 highly present in all layers of the epithelium. Cell apoptosis are sporadic). In injured untreated cornea further corneal disturbances developed: The expressions of matrix metalloproteinase 9 (MMP9) and proinflammatory cytokines, were high. At the end of experiment (on day 15) the injured untreated corneas were vascularized and numerous inflammatory cells were present in the corneal stroma.
dcterms:title
Suppression of alkali-induced oxidative injury in the cornea by mesenchymal stem cells growing on nanofiber scaffolds and transferred onto the damaged corneal surface Suppression of alkali-induced oxidative injury in the cornea by mesenchymal stem cells growing on nanofiber scaffolds and transferred onto the damaged corneal surface
skos:prefLabel
Suppression of alkali-induced oxidative injury in the cornea by mesenchymal stem cells growing on nanofiber scaffolds and transferred onto the damaged corneal surface Suppression of alkali-induced oxidative injury in the cornea by mesenchymal stem cells growing on nanofiber scaffolds and transferred onto the damaged corneal surface
skos:notation
RIV/00216208:11310/13:10189222!RIV14-MSM-11310___
n13:predkladatel
n21:orjk%3A11310
n3:aktivita
n8:Z n8:S n8:P n8:I
n3:aktivity
I, P(GAP301/11/1568), P(GAP304/11/0653), S, Z(AV0Z50390512), Z(MSM0021620858)
n3:cisloPeriodika
November
n3:dodaniDat
n7:2014
n3:domaciTvurceVysledku
n5:5695678 n5:2767198 n5:7357354
n3:druhVysledku
n17:J
n3:duvernostUdaju
n22:S
n3:entitaPredkladatele
n15:predkladatel
n3:idSjednocenehoVysledku
109055
n3:idVysledku
RIV/00216208:11310/13:10189222
n3:jazykVysledku
n16:eng
n3:klicovaSlova
real-time PCR; immunohistochemistry; central corneal thickness; rabbit mesenchymal stem cells; rabbit cornea; alkali-induced oxidative stress
n3:klicoveSlovo
n4:real-time%20PCR n4:rabbit%20cornea n4:rabbit%20mesenchymal%20stem%20cells n4:central%20corneal%20thickness n4:immunohistochemistry n4:alkali-induced%20oxidative%20stress
n3:kodStatuVydavatele
GB - Spojené království Velké Británie a Severního Irska
n3:kontrolniKodProRIV
[6A579ED7B054]
n3:nazevZdroje
Experimental Eye Research
n3:obor
n20:EC
n3:pocetDomacichTvurcuVysledku
3
n3:pocetTvurcuVysledku
9
n3:projekt
n14:GAP301%2F11%2F1568 n14:GAP304%2F11%2F0653
n3:rokUplatneniVysledku
n7:2013
n3:svazekPeriodika
116
n3:tvurceVysledku
Trošan, Peter Zajicová, Alena Syková, Eva Čejka, Čestmír Lencová, Anna Čejková, Jitka Holáň, Vladimír Javorková, Eliška Kubinová, Šárka
n3:wos
000327562500036
n3:zamer
n19:AV0Z50390512 n19:MSM0021620858
s:issn
0014-4835
s:numberOfPages
12
n6:doi
10.1016/j.exer.2013.10.002
n10:organizacniJednotka
11310