PC12 cells are known to degenerate within a few days of culture in serum-free medium, with nerve growth factor (NGF) and additional agents supporting their long-term survival under such conditions. In the present work, we adopted the serum-free paradigm of PC12 cells and investigated cell survival promoted by LiCl. We show here that Li+, with maximal activity in the 5-10 mM range, induces approximately 80% of short-term (2 days) cell survival, without stimulating proliferation in both naive and primed PC12 cells. Differently from NGF, lithium does not elicit morphological differentiation of the cells or trophic action. LiCl is furthermore effective in promoting the survival of A126-1 B2 cells (a variant of PC12 cells that is defective in cAMP-dependent Protein Kinase [PKA] activity) and of PC12 cells after downregulation of Protein Kinase C (PKC) levels. This suggests that PKA and PKC neither mediate nor are required for the survival-promoting effect of LiCl. Serumdeprived PC12 cells manifest an endonuclease activity that leads to internucleosomal cleavage of cellular DNA: the addition of lithium to the culture medium prevents fragmentation of PC12 cell DNA.
|Number of pages||9|
|Publication status||Published - 1993|
ASJC Scopus subject areas
- Pharmacology (medical)