Research reportNeuronal death, cytoplasmic calcium and internucleosomal DNA fragmentation: evidence for DNA fragments being released from cells
References (29)
- et al.
Apoptosis: mechanisms and roles in pathology
Int. Rev. Exp. Pathol.
(1991) - et al.
Practical aspects of the use aequorin as a calcium indicator: assay, preparation, microinjection, and interpretation of signals
Methods Enzymol.
(1978) - et al.
Evidence for early induction of calmodulin gene expression in lymphocytes undergoing glucocorticoid-mediated apoptosis
J. Biol. Chem.
(1991) - et al.
Measurement of platelet cytoplasmic ionized calcium concentration with aequorin and fluorescent indicators
Methods Enzymol.
(1989) - et al.
Calcium-activated DNA fragmentation in rat liver nuclei
J. Biol. Chem.
(1989) - et al.
Amyloid β-protein fragment 25–35 causes activation of cytoplasmic calcium in neurons
Biochem. Biophys. Res. Commun.
(1992) - et al.
Further studies on platelet-mediated neurotoxicity
Brain Res.
(1992) - et al.
Glutamate triggers internucleosomal DNA cleavage in neuronal cells
Biochem. Biophys. Res. Commun.
(1991) - et al.
Glucocorticoids activate a suicide process in thymocyte through an elevation of cytosolic Ca2+ concentration
Arch. Biochem. Biophys.
(1989) Naturally occurring cell death during neural development
Trends Neurosci.
(1985)
Measurement of growth and viability of cells in culture
Methods Enzymol.
Cell death: the significance of apoptosis
Int. Rev. Cytol.
Calcium ion concentrations and DNA fragmentation in target cell destruction by murine cloned cytotoxic T lymphocytes
J. Exp. Med.
Aurintricarboxylic acid rescues PC12 cells and sympathetic neurons from cell death caused by nerve growth factor deprivation: correlation with suppression of endonuclease activity
J. Cell Biol.
Cited by (64)
Cerebrolysin enhances spinal cord conduction and reduces blood-spinal cord barrier breakdown, edema formation, immediate early gene expression and cord pathology after injury
2020, Progress in Brain ResearchCitation Excerpt :Intracellular accumulation of high content of Ca2 + leads to disruption of ion hemostasis leading to neuronal stress and apoptosis (Mattson and Furukawa, 1996). Cerebrolysin reduces the intracellular accumulation of Ca2 + and minimizes apoptosis and enhanced cell survival (Gutmann et al., 2002; Joseph et al., 1993). Neuronal pathology following CNS ischemia alters neuronal morphology (Djuricic et al., 1994; Dux et al., 1992) due to energy exhaustion (Djuricic et al., 1994).
Phospholipase A<inf>2</inf>-mediated Ca<sup>2+</sup> influx by 2,2′,4,6-tetrachlorobiphenyl in PC12 cells
2002, Toxicology and Applied PharmacologyTetrahydrobiopterin Enhances Apoptotic PC12 Cell Death following Withdrawal of Trophic Support
2001, Journal of Biological ChemistryCitation Excerpt :These results suggest that hydrogen peroxide production cannot account for the enhancement of apoptotic death by elevating intracellular BH4 levels during withdrawal of trophic support. Since calcium influx can induce apoptotic PC12 cell death (10, 50, 51) and previous reports suggested that BH4 induces calcium influx (52, 53), we also tested the possibility that calcium influx is responsible for the enhancement of apoptotic PC12 cell death following sepiapterin treatment. Treatment with 1,2-bis(2-aminophenoxy)ethane-N,N,N′,N′-tetraacetic acid or with 1,2-bis(2-aminophenoxy)ethane-N,N,N′,N′-tetraacetic acid/acetoxymethylester (54) to chelate extracellular or intracellular calcium, respectively, failed to show a reversal of the sepiapterin-induced enhancement of DNA fragmentation and cell death (data not shown).
Aluminum-induced apoptosis in cultured astrocytes and its effect on calcium homeostasis
2001, Brain ResearchCitation Excerpt :Most studies, to date, have investigated the increase of intracellular Ca2+ as an early event in the activation of cell death in vivo and in vitro models of pathological conditions [3,4]. Induction of apoptosis by Ca2+ ionophores has been demonstrated in primary neuronal cell, the increase of intracellular calcium is thought to play a primary role in starting up the apoptotic pathway, probably through the activation of Ca2+/Mg2+-dependent endonucleases, which may be responsible for the fragmentation of DNA [9,32]. Changes in intracellular Ca2+ are important in regulation of astrocyte function as they are in neurons [5,8], either an elevation or a marked reduction in calcium can result in degeneration of astrocytes [3,14].
A population of PC12 cells that is initiating apoptosis can be rescued by nerve growth factor
2001, Molecular and Cellular Neuroscience