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Statements

Subject Item
n2:RIV%2F67985904%3A_____%2F12%3A00380414%21RIV13-GA0-67985904
rdf:type
n5:Vysledek skos:Concept
dcterms:description
Interdigital tissue regression is one of the most well-known examples of embryonic programmed cell death, providing the mechanism behind separation of developing digits. Caspases have been shown to play a key part in this process, with activated caspase-3 localized between the developing digits. In caspase-3 knock-out adult mice, however, the digits are completely separated with no webbing. In other mutants with defects in the apoptotic machinery, such as Apaf1 deficient mice, interdigital tissue regression is initially inhibited but the webbing eventually disappears as alternative/additional cell death mechanisms step in. In order to investigate whether a similar temporal effect occurs after loss of caspase-3, we have used an in vitro approach to inhibit caspase-3 at specific times during digit separation. Previous limb explant culture approaches have encountered problems with proper limb development in culture, and thus a modified technique was used. The new approach enables detailed observation of the effects of caspase-3 inhibition on interdigital regression. Using these methods, we show that caspase-3 inhibition caused a delay in the loss of interdigital tissue compared with control explants, similar to that observed in Apaf1 mutant mice. Along with immunohistochemistry, active caspase-3 positive cells of the interdigital vs. digital regions were measured by flow cytometry. Notably, activated caspase-3 in vivo was found not only in the interdigital mesenchyme but also in the TUNEL negative digit region, supporting a role for caspase-3 in nonapoptotic events Interdigital tissue regression is one of the most well-known examples of embryonic programmed cell death, providing the mechanism behind separation of developing digits. Caspases have been shown to play a key part in this process, with activated caspase-3 localized between the developing digits. In caspase-3 knock-out adult mice, however, the digits are completely separated with no webbing. In other mutants with defects in the apoptotic machinery, such as Apaf1 deficient mice, interdigital tissue regression is initially inhibited but the webbing eventually disappears as alternative/additional cell death mechanisms step in. In order to investigate whether a similar temporal effect occurs after loss of caspase-3, we have used an in vitro approach to inhibit caspase-3 at specific times during digit separation. Previous limb explant culture approaches have encountered problems with proper limb development in culture, and thus a modified technique was used. The new approach enables detailed observation of the effects of caspase-3 inhibition on interdigital regression. Using these methods, we show that caspase-3 inhibition caused a delay in the loss of interdigital tissue compared with control explants, similar to that observed in Apaf1 mutant mice. Along with immunohistochemistry, active caspase-3 positive cells of the interdigital vs. digital regions were measured by flow cytometry. Notably, activated caspase-3 in vivo was found not only in the interdigital mesenchyme but also in the TUNEL negative digit region, supporting a role for caspase-3 in nonapoptotic events
dcterms:title
The effect of caspase-3 inhibition on interdigital tissue regression in explant cultures of developing mouse limbs The effect of caspase-3 inhibition on interdigital tissue regression in explant cultures of developing mouse limbs
skos:prefLabel
The effect of caspase-3 inhibition on interdigital tissue regression in explant cultures of developing mouse limbs The effect of caspase-3 inhibition on interdigital tissue regression in explant cultures of developing mouse limbs
skos:notation
RIV/67985904:_____/12:00380414!RIV13-GA0-67985904
n5:predkladatel
n18:ico%3A67985904
n3:aktivita
n11:P n11:Z
n3:aktivity
P(ED2.1.00/03.0101), P(GA203/08/1680), P(IAA600450904), Z(AV0Z50450515)
n3:cisloPeriodika
4
n3:dodaniDat
n17:2013
n3:domaciTvurceVysledku
n4:3362051 n4:8914427 n4:4002032
n3:druhVysledku
n6:J
n3:duvernostUdaju
n20:S
n3:entitaPredkladatele
n16:predkladatel
n3:idSjednocenehoVysledku
132958
n3:idVysledku
RIV/67985904:_____/12:00380414
n3:jazykVysledku
n15:eng
n3:klicovaSlova
caspases; cell death; digitalization
n3:klicoveSlovo
n9:cell%20death n9:digitalization n9:caspases
n3:kodStatuVydavatele
KR - Korejská republika
n3:kontrolniKodProRIV
[BC60467541DC]
n3:nazevZdroje
Animal Cells and Systems
n3:obor
n14:EB
n3:pocetDomacichTvurcuVysledku
3
n3:pocetTvurcuVysledku
6
n3:projekt
n12:GA203%2F08%2F1680 n12:ED2.1.00%2F03.0101 n12:IAA600450904
n3:rokUplatneniVysledku
n17:2012
n3:svazekPeriodika
16
n3:tvurceVysledku
Tucker, A. S. Chlastáková, Ivana Doubek, J. Matalová, Eva Dubská, L. Kudělová, Judita
n3:wos
000308101700005
n3:zamer
n13:AV0Z50450515
s:issn
1976-8354
s:numberOfPages
7
n8:doi
10.1080/19768354.2012.678386