Tags

Type your tag names separated by a space and hit enter

Sphingosylphosphorylcholine induces apoptosis of endothelial cells through reactive oxygen species-mediated activation of ERK.
J Cell Biochem. 2007 Apr 15; 100(6):1536-47.JC

Abstract

Sphingosylphosphorylcholine (SPC) produces reactive oxygen species (ROS) in MS1 pancreatic islet endothelial cells. In the present study, we explored the physiological significance of the SPC-induced ROS generation in endothelial cells. SPC induced cell death of MS1 cells at higher than 10 microM concentration through a caspase-3-dependent pathway. SPC treatment induced sustained activation of an extracellular signal-regulated kinase (ERK), in contrast to transient activation of ERK in response to platelet-derived growth factor (PDGF)-BB, which stimulated proliferation of MS1 cells. Both the SPC-induced cell death and ERK activation were abolished by pretreatment of the cells with the MEK inhibitor U0126 or by overexpression of a dominant negative mutant of MEK1 (DN-MEK1). Pretreatment of the cells with N-acetylcysteine, an antioxidant, completely prevented the SPC-induced ROS generation, apoptosis, and ERK activation, whereas the ROS generation was not abrogated by treatment with U0126. Consistent with these results, SPC induced cell death of human umbilical vein endothelial cells (HUVECs) through ROS-mediated activation of ERK. These results suggest that the SPC-induced generation of ROS plays a crucial role in the cell death of endothelial cells through ERK-dependent pathway.

Authors+Show Affiliations

Medical Research Center for Ischemic Tissue Regeneration and Medical Research Institute, College of Medicine, Pusan National University, Busan 602-739, Republic of Korea.No affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

17131361

Citation

Jeon, Eun Su, et al. "Sphingosylphosphorylcholine Induces Apoptosis of Endothelial Cells Through Reactive Oxygen Species-mediated Activation of ERK." Journal of Cellular Biochemistry, vol. 100, no. 6, 2007, pp. 1536-47.
Jeon ES, Lee MJ, Sung SM, et al. Sphingosylphosphorylcholine induces apoptosis of endothelial cells through reactive oxygen species-mediated activation of ERK. J Cell Biochem. 2007;100(6):1536-47.
Jeon, E. S., Lee, M. J., Sung, S. M., & Kim, J. H. (2007). Sphingosylphosphorylcholine induces apoptosis of endothelial cells through reactive oxygen species-mediated activation of ERK. Journal of Cellular Biochemistry, 100(6), 1536-47.
Jeon ES, et al. Sphingosylphosphorylcholine Induces Apoptosis of Endothelial Cells Through Reactive Oxygen Species-mediated Activation of ERK. J Cell Biochem. 2007 Apr 15;100(6):1536-47. PubMed PMID: 17131361.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Sphingosylphosphorylcholine induces apoptosis of endothelial cells through reactive oxygen species-mediated activation of ERK. AU - Jeon,Eun Su, AU - Lee,Mi Jeong, AU - Sung,Sang-Min, AU - Kim,Jae Ho, PY - 2006/11/30/pubmed PY - 2007/7/31/medline PY - 2006/11/30/entrez SP - 1536 EP - 47 JF - Journal of cellular biochemistry JO - J Cell Biochem VL - 100 IS - 6 N2 - Sphingosylphosphorylcholine (SPC) produces reactive oxygen species (ROS) in MS1 pancreatic islet endothelial cells. In the present study, we explored the physiological significance of the SPC-induced ROS generation in endothelial cells. SPC induced cell death of MS1 cells at higher than 10 microM concentration through a caspase-3-dependent pathway. SPC treatment induced sustained activation of an extracellular signal-regulated kinase (ERK), in contrast to transient activation of ERK in response to platelet-derived growth factor (PDGF)-BB, which stimulated proliferation of MS1 cells. Both the SPC-induced cell death and ERK activation were abolished by pretreatment of the cells with the MEK inhibitor U0126 or by overexpression of a dominant negative mutant of MEK1 (DN-MEK1). Pretreatment of the cells with N-acetylcysteine, an antioxidant, completely prevented the SPC-induced ROS generation, apoptosis, and ERK activation, whereas the ROS generation was not abrogated by treatment with U0126. Consistent with these results, SPC induced cell death of human umbilical vein endothelial cells (HUVECs) through ROS-mediated activation of ERK. These results suggest that the SPC-induced generation of ROS plays a crucial role in the cell death of endothelial cells through ERK-dependent pathway. SN - 0730-2312 UR - https://www.unboundmedicine.com/medline/citation/17131361/Sphingosylphosphorylcholine_induces_apoptosis_of_endothelial_cells_through_reactive_oxygen_species_mediated_activation_of_ERK_ L2 - https://doi.org/10.1002/jcb.21141 DB - PRIME DP - Unbound Medicine ER -