Cobalt chloride-induced apoptosis and extracellular signal-regulated protein kinase 1/2 activation in rat C6 glioma cells

Seung Ju Yang, Jhin Soo Pyen, In Soo Lee, Hyeyoung Lee, Young Kwon Kim, Tae Ue Kim

Research output: Contribution to journalArticle

64 Citations (Scopus)

Abstract

Brain ischemia brings about hypoxic insults. Hypoxia is one of the major pathological factors inducing neuronal injury and central nervous system infection. We studied the involvement of mitogen-activated protein (MAP) kinase in hypoxia-induced apoptosis using cobalt chloride in C6 glioma cells. In vitro cytotoxicity of cobalt chloride was tested by MTT assay. Its IC50 value was 400 μM. The DNA fragment became evident after incubation of the cells with 300 μM cobalt chloride for 24 h. We also evidenced nuclear cleavage with morphological changes of the cells undergoing apoptosis with electron microscopy. Next, we examined the signal pathway of cobalt chloride-induced apoptosis in C6 cells. The activation of extracellular signal-regulated protein kinase 1/2 (ERK 1/2) started to increase at 1 h and was activated further at 6 h after treatment of 400 M cobalt chloride. In addition, pretreatment of PD98059 inhibited cobalt chloride-induced apoptotic cell morphology in Electron Microscopy. These results suggest that cobalt chloride is able to induce the apoptotic activity in C6 glioma cells, and its apoptotic mechanism may be associated with signal transduction via MAP kinase (ERK 1/2).

Original languageEnglish
Pages (from-to)480-486
Number of pages7
JournalJournal of Biochemistry and Molecular Biology
Volume37
Issue number4
Publication statusPublished - 2004 Jul 31

Fingerprint

Mitogen-Activated Protein Kinase 3
Glioma
Protein Kinases
Rats
Chemical activation
Apoptosis
Mitogen-Activated Protein Kinases
Electron microscopy
Signal Transduction
Electron Microscopy
Cells
Central Nervous System Infections
Signal transduction
Neurology
Cytotoxicity
cobaltous chloride
Brain Ischemia
Inhibitory Concentration 50
Assays
Brain

All Science Journal Classification (ASJC) codes

  • Biochemistry
  • Molecular Biology

Cite this

Yang, Seung Ju ; Pyen, Jhin Soo ; Lee, In Soo ; Lee, Hyeyoung ; Kim, Young Kwon ; Kim, Tae Ue. / Cobalt chloride-induced apoptosis and extracellular signal-regulated protein kinase 1/2 activation in rat C6 glioma cells. In: Journal of Biochemistry and Molecular Biology. 2004 ; Vol. 37, No. 4. pp. 480-486.
@article{b4af05d03d3a47daa012ff1f1a6b83c2,
title = "Cobalt chloride-induced apoptosis and extracellular signal-regulated protein kinase 1/2 activation in rat C6 glioma cells",
abstract = "Brain ischemia brings about hypoxic insults. Hypoxia is one of the major pathological factors inducing neuronal injury and central nervous system infection. We studied the involvement of mitogen-activated protein (MAP) kinase in hypoxia-induced apoptosis using cobalt chloride in C6 glioma cells. In vitro cytotoxicity of cobalt chloride was tested by MTT assay. Its IC50 value was 400 μM. The DNA fragment became evident after incubation of the cells with 300 μM cobalt chloride for 24 h. We also evidenced nuclear cleavage with morphological changes of the cells undergoing apoptosis with electron microscopy. Next, we examined the signal pathway of cobalt chloride-induced apoptosis in C6 cells. The activation of extracellular signal-regulated protein kinase 1/2 (ERK 1/2) started to increase at 1 h and was activated further at 6 h after treatment of 400 M cobalt chloride. In addition, pretreatment of PD98059 inhibited cobalt chloride-induced apoptotic cell morphology in Electron Microscopy. These results suggest that cobalt chloride is able to induce the apoptotic activity in C6 glioma cells, and its apoptotic mechanism may be associated with signal transduction via MAP kinase (ERK 1/2).",
author = "Yang, {Seung Ju} and Pyen, {Jhin Soo} and Lee, {In Soo} and Hyeyoung Lee and Kim, {Young Kwon} and Kim, {Tae Ue}",
year = "2004",
month = "7",
day = "31",
language = "English",
volume = "37",
pages = "480--486",
journal = "BMB Reports",
issn = "1976-6696",
publisher = "The Biochemical Society of the Republic of Korea",
number = "4",

}

Cobalt chloride-induced apoptosis and extracellular signal-regulated protein kinase 1/2 activation in rat C6 glioma cells. / Yang, Seung Ju; Pyen, Jhin Soo; Lee, In Soo; Lee, Hyeyoung; Kim, Young Kwon; Kim, Tae Ue.

In: Journal of Biochemistry and Molecular Biology, Vol. 37, No. 4, 31.07.2004, p. 480-486.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Cobalt chloride-induced apoptosis and extracellular signal-regulated protein kinase 1/2 activation in rat C6 glioma cells

AU - Yang, Seung Ju

AU - Pyen, Jhin Soo

AU - Lee, In Soo

AU - Lee, Hyeyoung

AU - Kim, Young Kwon

AU - Kim, Tae Ue

PY - 2004/7/31

Y1 - 2004/7/31

N2 - Brain ischemia brings about hypoxic insults. Hypoxia is one of the major pathological factors inducing neuronal injury and central nervous system infection. We studied the involvement of mitogen-activated protein (MAP) kinase in hypoxia-induced apoptosis using cobalt chloride in C6 glioma cells. In vitro cytotoxicity of cobalt chloride was tested by MTT assay. Its IC50 value was 400 μM. The DNA fragment became evident after incubation of the cells with 300 μM cobalt chloride for 24 h. We also evidenced nuclear cleavage with morphological changes of the cells undergoing apoptosis with electron microscopy. Next, we examined the signal pathway of cobalt chloride-induced apoptosis in C6 cells. The activation of extracellular signal-regulated protein kinase 1/2 (ERK 1/2) started to increase at 1 h and was activated further at 6 h after treatment of 400 M cobalt chloride. In addition, pretreatment of PD98059 inhibited cobalt chloride-induced apoptotic cell morphology in Electron Microscopy. These results suggest that cobalt chloride is able to induce the apoptotic activity in C6 glioma cells, and its apoptotic mechanism may be associated with signal transduction via MAP kinase (ERK 1/2).

AB - Brain ischemia brings about hypoxic insults. Hypoxia is one of the major pathological factors inducing neuronal injury and central nervous system infection. We studied the involvement of mitogen-activated protein (MAP) kinase in hypoxia-induced apoptosis using cobalt chloride in C6 glioma cells. In vitro cytotoxicity of cobalt chloride was tested by MTT assay. Its IC50 value was 400 μM. The DNA fragment became evident after incubation of the cells with 300 μM cobalt chloride for 24 h. We also evidenced nuclear cleavage with morphological changes of the cells undergoing apoptosis with electron microscopy. Next, we examined the signal pathway of cobalt chloride-induced apoptosis in C6 cells. The activation of extracellular signal-regulated protein kinase 1/2 (ERK 1/2) started to increase at 1 h and was activated further at 6 h after treatment of 400 M cobalt chloride. In addition, pretreatment of PD98059 inhibited cobalt chloride-induced apoptotic cell morphology in Electron Microscopy. These results suggest that cobalt chloride is able to induce the apoptotic activity in C6 glioma cells, and its apoptotic mechanism may be associated with signal transduction via MAP kinase (ERK 1/2).

UR - http://www.scopus.com/inward/record.url?scp=4444293631&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=4444293631&partnerID=8YFLogxK

M3 - Article

C2 - 15469737

AN - SCOPUS:4444293631

VL - 37

SP - 480

EP - 486

JO - BMB Reports

JF - BMB Reports

SN - 1976-6696

IS - 4

ER -