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.
Highlights
Axons are guided to their targets during development by a combination of contact mediated and diffusible cues that are either attractive or repulsive (Paves and Saarma, 1997), and the growth cone at the nerve fiber terminus is believed to guide the axon by sampling the environment for either positive or negative signals using filopodial and lamellar protrusions (Goodman, 1996; Zheng et al, 1996; Mueller, 1999)
These results suggest that phospholipase D2 (PLD2), but not PLD1, is involved in the LPC-stimulated Phospholipase D (PLD) activity in PC12 cells
We demonstrated that PLD2 in PC12 cells was activated by LPC treatment
Summary
Axons are guided to their targets during development by a combination of contact mediated and diffusible cues that are either attractive or repulsive (Paves and Saarma, 1997), and the growth cone at the nerve fiber terminus is believed to guide the axon by sampling the environment for either positive or negative signals using filopodial and lamellar protrusions (Goodman, 1996; Zheng et al, 1996; Mueller, 1999). Lysophosphatidylcholine (LPC) is a major plasma lipid component that is generated by phospholipase A2 (PLA2)-mediated hydrolysis of phosphatidylcholine under physiological and pathological conditions (Prokazova et al, 1998; Macphee, 2001), and secretory PLA2 has been demonstrated to stimulate neuritogenesis through generation of LPC in PC12 cells (Ikeno et al, 2005). These results suggest that LPC plays a pivotal role in axonal outgrowth and guidance by regulating neuritogeneis.
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