Does overexpression of nuclear distribution protein ( hNUDC ) cause pro-apoptosis and differentiation in Dami megakaryocytes?
Functional studies using adenovirus-mediated hNUDC overexpression led to inhibition of megakaryocyte proliferation via cell cycle arrest in G2/M transition phase. This process could have been be mediated by upregulation of p21 and downregulation of its downstream targets, including cyclin B1, cyclin B2 and c-myc. Enhanced apoptosis in turn ensued, characterized by increased caspase-3 activation, upregulation of pro-apoptotic Bax and downregulation of anti-apoptotic Bcl-2. Furthermore, hNUDC overexpression elevated the level of megakaryocyte maturation, associated with increased polyploidy, cell morphological changes and increased expression of cell surface differentiation markers, including CD10, CD44, CD41 and CD61. Our results further suggest that the ERK signalling pathway was involved in hNUDC overexpression-induced apoptosis. Taken together, this study provides experimental evidence for overexpression of hNUDC in Dami cells and suggests that activation of apoptotic machinery may be involved in megakaryocytic differentiation.
Section the pain pathways carried by sympathetic lumbar rami communicantes for refractory low back pain improved 22 % of patients at the last follow-up of 29 months.