Dopamine-induced programmed cell death in mouse thymocytes

Offen, Daniel; Ziv, Ilan; Gorodin, Svetlana; Barzilai, Ari; Malik, Zvi; Melamed, Eldad

doi:10.1016/0167-4889(95)00075-4

Cited by 116 publications

(78 citation statements)

References 20 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…What has separated sodium from potassium during apoptosis is the occurrence of an early increase in sodium during the cell death process. Several initial studies on ions and apoptosis have reported this early increase in intracellular sodium [85][86][87][88]. Additionally, we have shown that apoptotic cells have a significant increase in intracellular sodium that occurs prior to the dramatic loss of cell volume with a variety of apoptotic agents in Jurkat T-cells [89].…”

Section: Sodium As a Signal During Apoptosismentioning

confidence: 89%

Cell shrinkage and monovalent cation fluxes: Role in apoptosis

Bortner

Cidlowski

2007

Archives of Biochemistry and Biophysics

228

193

View full text Add to dashboard Cite

The loss of cell volume or cell shrinkage has been a morphological hallmark of the programmed cell death process known as apoptosis. This isotonic loss of cell volume has recently been term apoptotic volume decrease or AVD to distinguish it from inherent volume regulatory responses that occurs in cells under anisotonic conditions. Recent studies examining the intracellular signaling pathways that result in this unique cellular characteristic have determined that a fundamental movement of ions, particularly monovalent ions, underlie the AVD process and plays an important role on controlling the cell death process. An efflux of intracellular potassium was shown to be a critical aspect of the AVD process, as preventing this ion loss could protect cells from apoptosis. However, potassium plays a complex role as a loss of intracellular potassium has also been shown to be beneficial to the health of the cell. Additionally, the mechanisms that a cell employs to achieve this loss of intracellular potassium vary depending on the cell type and stimulus used to induce apoptosis, suggesting multiple ways exist to accomplish the same goal of AVD. Additionally, sodium and chloride have been shown to play a vital role during cell death in both the signaling and control of AVD in various apoptotic model systems. This review examines the relationship between this morphological change and intracellular monovalent ions during apoptosis.

show abstract

Section: Sodium As a Signal During Apoptosismentioning

confidence: 89%

Cell shrinkage and monovalent cation fluxes: Role in apoptosis

Bortner

Cidlowski

2007

Archives of Biochemistry and Biophysics

228

193

View full text Add to dashboard Cite

show abstract

“…Dopamine and other catecholamines in micromolar concentrations induce degeneration of cultured cortical cells (32). In addition, sympathetic neurons and thymocytes exposed to high concentrations of dopamine undergo apoptosis characterized by cell body shrinkage, nuclear chromatin condensation, and internucleosomal DNA fragmentation (29,36). Metabolism of dopamine by monoamine oxidase or nonenzymatic autooxidation results in production of hydrogen peroxide and then free radicals, suggesting that dopamine induces oxidative neuronal death (14,28).…”

Section: R 1997 Academic Pressmentioning

confidence: 99%

Attenuation of Oxidative Neuronal Necrosis by a Dopamine D1 Agonist in Mouse Cortical Cell Cultures

Noh

Gwag

1997

Experimental Neurology

View full text Add to dashboard Cite

“…Also, Na + deprivation should lead to a reduction in the intracellular Na + concentration. However, a decrease in the cytosolic Na + level does not provide a necessary condition for apoptosis induction because an increase in the intracellular Na + concentration was found to be coupled to apoptosis in several cell types [15][16][17][18]. Thus it is highly possible that persistent cell shrinkage per se and/or some signal downstream to shrinkage may be a causative factor(s) for apoptosis induction in HeLa cells exposed to Na + -free solution.…”

Section: Reverse-mode Operation Of Nkcc and Ncx Is Involved In Apoptomentioning

confidence: 99%

Normotonic Cell Shrinkage Induced by Na+ Deprivation Results in Apoptotic Cell Death in Human Epithelial HeLa Cells

Nukui¹,

Shimizu²,

Okada³

2006

J. Physiol. Sci

View full text Add to dashboard Cite

Apoptosis is a major form of cell death that occurs in response to a variety of signals in both physiological and pathological situations. A hallmark of apoptosis is normotonic cell shrinkage, called apoptotic volume decrease (AVD), the process of which involves fluxes of K + , Cl − , and Na + . Na + influx was suggested to be required in Fas-induced apoptosis in human Jurkat T cells, whereas Na + efflux was found to be associated with AVD and apoptosis in human HL-60 cells. Here we examined the effects of extracellular Na + deprivation on cell volume and viability in human epithelial HeLa cells. The incubation of HeLa cells in normotonic Na + -free Ringer solution resulted in persistent cell shrinkage after ≥30 min and reduction in cell viability after ≥1 h. After exposure to Na + -free solution for 5 h, a marked reduction in cell viability was found to be associated with an activation of caspase-3 without showing significant LDH release, indicating that the cells underwent apoptosis but not necrosis. Na + deprivation-induced cell shrinkage and apoptotic cell death were significantly inhibited by a blocker of Na + -K + -2Cl − cotransporter (NKCC) or of the reverse-mode operation of Na + /Ca 2+ exchanger (NCX), but not by a blocker of Na + /H + exchanger (NHE). Therefore it is concluded that Na + deprivation causes persistent cell shrinkage resulting from Na + efflux mainly via NKCC and NCX and thereafter leads to apoptotic death of HeLa cells. It is also suggested that normotonic cell shrinkage per se, if persistent, provides a sufficient condition for apoptosis induction.Key words: apoptosis, Na + efflux, apoptotic volume decrease, normotonic cell shrinkage.Apoptosis is an essential process involved in normal somatic cell turnover, embryonic development, and metamorphosis, and inappropriate apoptosis is implicated in the pathogenesis of degenerative diseases, ischemic damage, autoimmune disorders, and cancer. A major hallmark of the early-phase process of apoptosis is normotonic whole cell shrinkage [1]. The apoptotic volume decrease (AVD) is attained by water exit driven by an efflux of osmolytes, including K + and Cl − , and is an essential event leading to apoptotic cell death under stimulation with a variety of apoptosis inducers [2][3][4].Recently, we have demonstrated that exposure to normotonic low Cl − solution induces persistent cell shrinkage and thereafter apoptotic death in U937 and HeLa cells even without the application of any apoptosis inducer [5]. These results suggest that ion efflux mediated by an outward-directed operation of Cl − transporters results in normotonic cell shrinkage leading to apoptosis. Thus it is possible that exposure to Na + -free solution also gives rise to persistent normotonic cell shrinkage resulting in apoptosis. The first purpose of the present study was to test this possibility. An imposition of an electrochemical driving force for passive Na + efflux may facilitate the outward operations of Na + -K + -2Cl − cotransporter (NKCC) and Na + / H + exchanger (NH...

show abstract

Dopamine-induced programmed cell death in mouse thymocytes

Cited by 116 publications

References 20 publications

Cell shrinkage and monovalent cation fluxes: Role in apoptosis

Cell shrinkage and monovalent cation fluxes: Role in apoptosis

Attenuation of Oxidative Neuronal Necrosis by a Dopamine D1 Agonist in Mouse Cortical Cell Cultures

Normotonic Cell Shrinkage Induced by Na+ Deprivation Results in Apoptotic Cell Death in Human Epithelial HeLa Cells

Contact Info

Product

Resources

About