Inhibition of high glucose-induced protein mono-ADP-ribosylation restores neuritogenesis and sodium-pump activity in SY5Y neuroblastoma cells
✍ Scribed by Anna Maria Di Giulio; Elena Lesma; Elena Germani; Alfredo Gorio
- Publisher
- John Wiley and Sons
- Year
- 1999
- Tongue
- English
- Weight
- 139 KB
- Volume
- 57
- Category
- Article
- ISSN
- 0360-4012
No coin nor oath required. For personal study only.
✦ Synopsis
The exposure of SY5Y neuroblastoma cells to high concentrations of glucose, fructose, or galactose is an experimental model commonly used for in vitro evaluation of typical neuronal alterations observed in diabetes mellitus. In the present study, we observed that 2 weeks of exposure to high carbohydrate concentrations caused both a significant impairment in neurite formation induced by supplementation of retinoic acid or by subtraction of fetal calf serum to the culture medium and a marked reduction in Na ؉ -K ؉ -ATPase activity. However, only the exposure to high millimoles of glucose caused an enhancement of mono-ADP-ribosylation, typical of diabetes mellitus, affecting at leat five proteins. The concomitant exposure to high glucose and to silybin, a mono-ADPribosylation inhibitor, normalized the extent of ADPribosylation of the five proteins and counteracted the inhibitory effects of high glucose on Na ؉ -pump activity and on neuritogenesis. Conversely, the supplementation of silybin did not prevent fructose and galactose inhibitory effects on Na ؉ -pump activity and neurite formation. These data confirm those of previous reports suggesting a link between excessive protein mono-ADP-ribosylation and the onset of diabetic complications such as diabetic neuropathy.