Stimuli that induce a cholinergic neuronal phenotype of NG108-15 cells upregulate ChAT and VAChT mRNAs but fail to increase VAChT protein

The Increase of Choline Acetyltransferase Activity by Docosahexaenoic Acid in NG108-15 Cells Grown in Serum-free Medium is Independent of its Effect on Cell Growth

“…Effects of DHA on cell growth and ChAT activity in serum-free medium Differentiation of NG108-15 cells induced by 100 nM dexamethasone and 0.2 mM dibutyryl-cAMP in presence of serum increased ChAT activity more than five times and attenuated cell growth estimated as a decrease of protein content by 34% (Table 1) in line with previous findings [12,13]. Deceleration of cell growth was connected with strong reduction of executioner caspase-3 activity.…”

“…For all other experiments, 20,000 cells were seeded into each well of 24-well-plate and grown in 2 ml of basal or serum-free Dulbecco's modified Eagle's medium. Differentiation of cells was induced by 0.2 mM dibutyrylcAMP and 100 nM dexamethasone [12][13][14].…”

“…We have reported previously that differentiation of NG108-15 cells induced by cAMP and dexamethasone leads to morphological differentiation accompanied by a marked enhancement of the cholinergic gene locus transcription, the expression of ChAT activity, and depolarizationinduced calcium influx through neuronal voltageoperated calcium channels [12][13][14]. In the present experiments we utilized these cells to investigate a presumed effect of DHA on the expression of their cholinergic phenotype represented by ChAT activity.…”

Immuno-detection of OCTN1 (SLC22A4) in HeLa cells and characterization of transport function

“…A very low if any level of the VAChT mRNA was detected indicating that the corresponding protein is not expressed. It has to be evidenced also that the presence of VAChT mRNA in a neuroblastoma cell line did not account for expression of VAChT protein [1]. Moreover, VAChT is a vesicular transporter which transport mechanism relies on driving the acetylcholine accumulation by protons, which is difficult to occur on the plasma membrane [12].…”

Asymmetric regulation by estrogen at the cholinergic gene locus in differentiated NG108-15 neuronal cells

“…The NG108-15 cells are a hybrid cell line constructed by somatic fusion of rat C6 glioma cells and mouse N18TG2 neuroblastoma cells. N18TG2 cells themselves do not express the differentiated phenotypes in the presence of RA (Bignami et al 1997), but NG108-15 and N18TG2 treated with a medium conditioned over C6 cells can differentiate by retinoic acid into functional cholinergic cells (Diebler et al 1998;Dolezal et al 2001;Castell et al 2002), indicating that the differentiation of N18TG2 neuroblastoma requires the cooperation of C6 glioma. The possibility remains that E 2 acted directly or indirectly on differentiation-inducing factor(s) derived from C6 glioma, and prompted further increase of ChAT gene expression.…”