Vol 51, No 4 (2013)
Original paper
Submitted: 2014-02-05
Accepted: 2014-02-05
Published online: 2014-02-05
Relationships between calpains and glutamate- or kainate-induced apoptosis in Xenopus laevis tadpoles
Claire Brun, Elara Moudilou, Caroline Bouchot, Lucie Abrouk-Vérot, Jean-Marie Exbrayat
DOI: 10.5603/FHC.2013.0041
·
Folia Histochem Cytobiol 2013;51(4):300-311.
Vol 51, No 4 (2013)
ORIGINAL PAPERS
Submitted: 2014-02-05
Accepted: 2014-02-05
Published online: 2014-02-05
Abstract
Abstract: Cell glutamate-damage induced by overstimulation of ionotropic receptors is initiated by modification of the intracellular Ca2+ homeostasis and the concomitant activation of Ca2+-dependent cysteine proteases, the calpain and caspase families. The resultant cleavage of target molecules mediates a critical function in the execution of the cell death. In this work, we investigated relationships between the activity of calpain and glutamate-orkainate-induced apoptosis in several organs of Xenopus laevis tadpole. Animals (stage 48) were incubated for 3 hours with glutamate (30–120 mM) or kainate (0.015–0.75 mM) and the rise of both apoptosis and calpain was observed in several organs. Our results indicated that glutamate (120 mM) or kainate (0.15 mM) exposure induced cell death with apoptotic features. The toxic effects of drugs into the organs were variable. Apoptosis was probably not the only form of cell death and option of necrosis or apoptosis was depending on the stimulation degree of the receptor, i.e. the receptor type, intensity and time course of molecule exposure. The increase of ubiquitous calpain was not correlated with the peak of apoptosis, suggesting the role of calpain in cell death was complex: calpain and caspase pathways were tightly interrelated in the glutamate- or kainate-induced cell death and the contribution of calpain to another type of death than apoptosis was perhaps preferred.
Abstract
Abstract: Cell glutamate-damage induced by overstimulation of ionotropic receptors is initiated by modification of the intracellular Ca2+ homeostasis and the concomitant activation of Ca2+-dependent cysteine proteases, the calpain and caspase families. The resultant cleavage of target molecules mediates a critical function in the execution of the cell death. In this work, we investigated relationships between the activity of calpain and glutamate-orkainate-induced apoptosis in several organs of Xenopus laevis tadpole. Animals (stage 48) were incubated for 3 hours with glutamate (30–120 mM) or kainate (0.015–0.75 mM) and the rise of both apoptosis and calpain was observed in several organs. Our results indicated that glutamate (120 mM) or kainate (0.15 mM) exposure induced cell death with apoptotic features. The toxic effects of drugs into the organs were variable. Apoptosis was probably not the only form of cell death and option of necrosis or apoptosis was depending on the stimulation degree of the receptor, i.e. the receptor type, intensity and time course of molecule exposure. The increase of ubiquitous calpain was not correlated with the peak of apoptosis, suggesting the role of calpain in cell death was complex: calpain and caspase pathways were tightly interrelated in the glutamate- or kainate-induced cell death and the contribution of calpain to another type of death than apoptosis was perhaps preferred.
Keywords
calpain; apoptosis; ecotoxicity; glutamate receptors; calcium; Xenopus laevis
Title
Relationships between calpains and glutamate- or kainate-induced apoptosis in Xenopus laevis tadpoles
Journal
Folia Histochemica et Cytobiologica
Issue
Vol 51, No 4 (2013)
Article type
Original paper
Pages
300-311
Published online
2014-02-05
Page views
1585
Article views/downloads
1784
DOI
10.5603/FHC.2013.0041
Bibliographic record
Folia Histochem Cytobiol 2013;51(4):300-311.
Keywords
calpain
apoptosis
ecotoxicity
glutamate receptors
calcium
Xenopus laevis
Authors
Claire Brun
Elara Moudilou
Caroline Bouchot
Lucie Abrouk-Vérot
Jean-Marie Exbrayat