Skip Navigation

This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Request Permissions
Google Scholar
Right arrow Articles by Araki, S.
Right arrow Articles by Hayashi, H.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Araki, S.
Right arrow Articles by Hayashi, H.
Social Bookmarking
 Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

J. Biochem, 1994, Vol. 115, No. 2 245-247
© 1994 Japanese Biochemical Society


research-article

Programmed Cell Death in Response to Alkyllysophospholipids in Endothelial Cells1

Satohiko Araki*, Ikuo Tsuna*, Kazuhiko Kaji** and Hiroshi Hayashi*

*Sugashuna MBL, School of Science, Nagoya University Sugashima, Toba, Mie 517
**Tokyo Metropolitan Institute of Gerontology Itabashi-ku, Tokyo 173

Addition of the alkyllysophospholipid ET16-OMe, a putative antitumor drug, to the culture medium of human vascular endothelial cells resulted in apoptotic cell death. The death was characterized as programmed cell death since the process was inhibited by the addition of an inhibitor of protein synthesis. The mechanism responsible for apoptosis induced by alkyllysophospholipid has unique characteristics, as compared to those of apoptosis induced by other antitumor drugs, since the drug caused fragmentation of dying cells and its effect could be overcome by the presence of a survival factor, namely, fibroblast growth factor.

1This work was supported by a grant from the Ishida Foundation. Abbreviations: ALPs, alkyllysophospholipids, CHX, cycloheximide; ET16-OMe, rac-1-hexadecyl 2-methyl phosphatidylchohne; FBS, fetal bovine serum; FGF, fibroblast growth factor; LPC, 1-hexadecanoyl lysophosphatidylcholine; PAF, sn- 1-hexadecyl 2-acetyl phosphatidylcholine; VEC, vascular endothelial cells.


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
Am. J. Physiol. Heart Circ. Physiol.Home page
K. L. Houck, T. E. Fox, L. Sandirasegarane, and M. Kester
Ether-linked diglycerides inhibit vascular smooth muscle cell growth via decreased MAPK and PI3K/Akt signaling
Am J Physiol Heart Circ Physiol, October 1, 2008; 295(4): H1657 - H1668.
[Abstract] [Full Text] [PDF]


Home page
J. Biol. Chem.Home page
I. Baburina and S. Jackowski
Apoptosis Triggered by 1-O-Octadecyl-2-O-methyl-rac-glycero-3-phosphocholine Is Prevented by Increased Expression of CTP:Phosphocholine Cytidylyltransferase
J. Biol. Chem., January 23, 1998; 273(4): 2169 - 2173.
[Abstract] [Full Text] [PDF]


Home page
J. Biol. Chem.Home page
A. Mandal, Y. Wang, P. Ernsberger, and M. Kester
Interleukin-1-induced Ether-linked Diglycerides Inhibit Calcium-insensitive Protein Kinase C Isotypes. IMPLICATIONS FOR GROWTH SENESCENCE
J. Biol. Chem., August 8, 1997; 272(32): 20306 - 20311.
[Abstract] [Full Text] [PDF]



Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.