Lysophosphatidylcholine suppresses apoptosis and induces neurite outgrowth in PC12 cells through activation of phospholipase D2.
- Author:
Doo Hee YUN
1
;
Eun Su JEON
;
Sang Min SUNG
;
Sung Ho RYU
;
Jae Ho KIM
Author Information
1. Research Center for Ischemic Tissue Regeneration and Medical Research Institute, College of Medicine, Pusan National University, Busan 602-739, Korea. jhkimst@pusan.ac.kr
- Publication Type:Original Article ; Research Support, Non-U.S. Gov't
- Keywords:
apoptosis;
lysophosphatidylcholines;
neurites;
PC12 cells;
phospholipase D2
- MeSH:
Starvation;
Rats;
Phospholipase D/antagonists & inhibitors/*metabolism;
PC12 Cells;
Neurites/*drug effects;
Lysophosphatidylcholines/*pharmacology;
Cell Survival/drug effects;
Apoptosis/*drug effects;
Animals
- From:Experimental & Molecular Medicine
2006;38(4):375-384
- CountryRepublic of Korea
- Language:English
-
Abstract:
Lysophosphatidylcholine (LPC) is a bioactive lipid generated by phospholipase A2-mediated hydrolysis of phosphatidylcholine. In the present study, we demonstrate that LPC stimulates phospholipase D2 (PLD2) activity in rat pheochromocytoma PC12 cells. Serum deprivation induced cell death of PC12 cells, as demonstrated by decreased viability, DNA fragmentation, and increased sub-G1 fraction of cell cycle. LPC treatment protected PC12 cells partially from the cell death and induced neurite outgrowth of the cells. Overexpression of PLD2 drastically enhanced the LPC-induced inhibition of apoptosis and neuritogenesis. Pretreatment of the cells with 1-butanol, a PLD inhibitor, completely abrogated the LPC-induced inhibition of apoptosis and neurite outgrowth in PC12 cells overexpressing PLD2. These results indicate that LPC possesses the neurotrophic effects, such as anti-apoptosis and neurite outgrowth, through activation of PLD2.
