Relationship between autophagy and apoptosis in Paracentrotus lividus embryos cadmium exposed

Maria Carmela Roccheri, Roberto Chiarelli, Giovanni Morici, Maria Agnello

Risultato della ricerca: Other

Abstract

Sea urchin embryo is a developmental model that offers an excellent opportunity to investigate the possible adaptive response of cells exposed to different stress during differentiation. We previously demonstrated that cadmium treatment triggers the accumulation of metal in embryonic cells and the activation of defense systems depending on concentration and exposure time, through the synthesis of heat shock proteins and/or the initiation of apoptosis.Using several techniques to detect autophagy (neutral red, acridine orange and LC3-detection) we demonstrated that Cd-exposed P. lividus embryos adopt this process as an additional stratagem to safeguard the developmental program. In particular we observed that embryos treated at subletal Cd concentration activate a massive autophagic response after 18 h, which decreases between 21 and 24 h, in the opposite of apoptotic process.In order to investigate a possible temporal relationship between autophagy and apoptosis, we tested apoptotic signals by TUNEL and immunofluorescence in situ assays of cleaved caspase-3. Quantitative analysis has shown that embryos activate a massive apoptosis after 24 h of Cd-exposure. erefore a functional relationship between autophagy and apoptosis was estimated evaluating apoptotic signals in Cd-exposed embryos, upon treatment with the autophagic inhibitor 3-methyladenine. We found that the inhibition of autophagy produced a contemporaneous reduction of apoptotic signals, suggesting that the two phenomena are functionally related. In effect using methylpyruvate, a cell-permeable substrate for ATP production, apoptotic signals were substantially restored. ese data could be explained considering that autophagy could energetically contribute to apoptotic execution through its catabolic role.
Lingua originaleEnglish
Pagine109-109
Numero di pagine1
Stato di pubblicazionePublished - 2011

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Paracentrotus lividus
autophagy
cadmium
embryo (animal)
apoptosis
acridine orange
cells
caspase-3
Echinoidea
heat shock proteins
exposure duration
quantitative analysis
metals
synthesis
assays

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title = "Relationship between autophagy and apoptosis in Paracentrotus lividus embryos cadmium exposed",
abstract = "Sea urchin embryo is a developmental model that offers an excellent opportunity to investigate the possible adaptive response of cells exposed to different stress during differentiation. We previously demonstrated that cadmium treatment triggers the accumulation of metal in embryonic cells and the activation of defense systems depending on concentration and exposure time, through the synthesis of heat shock proteins and/or the initiation of apoptosis.Using several techniques to detect autophagy (neutral red, acridine orange and LC3-detection) we demonstrated that Cd-exposed P. lividus embryos adopt this process as an additional stratagem to safeguard the developmental program. In particular we observed that embryos treated at subletal Cd concentration activate a massive autophagic response after 18 h, which decreases between 21 and 24 h, in the opposite of apoptotic process.In order to investigate a possible temporal relationship between autophagy and apoptosis, we tested apoptotic signals by TUNEL and immunofluorescence in situ assays of cleaved caspase-3. Quantitative analysis has shown that embryos activate a massive apoptosis after 24 h of Cd-exposure. erefore a functional relationship between autophagy and apoptosis was estimated evaluating apoptotic signals in Cd-exposed embryos, upon treatment with the autophagic inhibitor 3-methyladenine. We found that the inhibition of autophagy produced a contemporaneous reduction of apoptotic signals, suggesting that the two phenomena are functionally related. In effect using methylpyruvate, a cell-permeable substrate for ATP production, apoptotic signals were substantially restored. ese data could be explained considering that autophagy could energetically contribute to apoptotic execution through its catabolic role.",
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T1 - Relationship between autophagy and apoptosis in Paracentrotus lividus embryos cadmium exposed

AU - Roccheri, Maria Carmela

AU - Chiarelli, Roberto

AU - Morici, Giovanni

AU - Agnello, Maria

PY - 2011

Y1 - 2011

N2 - Sea urchin embryo is a developmental model that offers an excellent opportunity to investigate the possible adaptive response of cells exposed to different stress during differentiation. We previously demonstrated that cadmium treatment triggers the accumulation of metal in embryonic cells and the activation of defense systems depending on concentration and exposure time, through the synthesis of heat shock proteins and/or the initiation of apoptosis.Using several techniques to detect autophagy (neutral red, acridine orange and LC3-detection) we demonstrated that Cd-exposed P. lividus embryos adopt this process as an additional stratagem to safeguard the developmental program. In particular we observed that embryos treated at subletal Cd concentration activate a massive autophagic response after 18 h, which decreases between 21 and 24 h, in the opposite of apoptotic process.In order to investigate a possible temporal relationship between autophagy and apoptosis, we tested apoptotic signals by TUNEL and immunofluorescence in situ assays of cleaved caspase-3. Quantitative analysis has shown that embryos activate a massive apoptosis after 24 h of Cd-exposure. erefore a functional relationship between autophagy and apoptosis was estimated evaluating apoptotic signals in Cd-exposed embryos, upon treatment with the autophagic inhibitor 3-methyladenine. We found that the inhibition of autophagy produced a contemporaneous reduction of apoptotic signals, suggesting that the two phenomena are functionally related. In effect using methylpyruvate, a cell-permeable substrate for ATP production, apoptotic signals were substantially restored. ese data could be explained considering that autophagy could energetically contribute to apoptotic execution through its catabolic role.

AB - Sea urchin embryo is a developmental model that offers an excellent opportunity to investigate the possible adaptive response of cells exposed to different stress during differentiation. We previously demonstrated that cadmium treatment triggers the accumulation of metal in embryonic cells and the activation of defense systems depending on concentration and exposure time, through the synthesis of heat shock proteins and/or the initiation of apoptosis.Using several techniques to detect autophagy (neutral red, acridine orange and LC3-detection) we demonstrated that Cd-exposed P. lividus embryos adopt this process as an additional stratagem to safeguard the developmental program. In particular we observed that embryos treated at subletal Cd concentration activate a massive autophagic response after 18 h, which decreases between 21 and 24 h, in the opposite of apoptotic process.In order to investigate a possible temporal relationship between autophagy and apoptosis, we tested apoptotic signals by TUNEL and immunofluorescence in situ assays of cleaved caspase-3. Quantitative analysis has shown that embryos activate a massive apoptosis after 24 h of Cd-exposure. erefore a functional relationship between autophagy and apoptosis was estimated evaluating apoptotic signals in Cd-exposed embryos, upon treatment with the autophagic inhibitor 3-methyladenine. We found that the inhibition of autophagy produced a contemporaneous reduction of apoptotic signals, suggesting that the two phenomena are functionally related. In effect using methylpyruvate, a cell-permeable substrate for ATP production, apoptotic signals were substantially restored. ese data could be explained considering that autophagy could energetically contribute to apoptotic execution through its catabolic role.

KW - Apoptosis

KW - Autophagy

KW - Cadmium

KW - Sea urchin embryos

KW - stress

UR - http://hdl.handle.net/10447/59867

UR - http://abcd2011.azuleon.org/_docs/Abstract_Book_ABCD2011.pdf

M3 - Other

SP - 109

EP - 109

ER -