Nicotinamide (NAM) a form of vitamin B3, is an essential precursor of NAD. This dinucleotide (pyridine nucleotide) participates in the regulation of fundamental processes including transcription, cell cycle progression and DNA repair. Here we assessed the effect of NAM on myeloid differentiation of the IL-3 dependent, multipotent hematopoietic progenitor cell line FDCP-Mix. We found that NAM reduces the pSTAT5 signaling response, cell cycling and self-renewal potential. It initiates an atypical program of myeloid differentiation that results in the emergence of granulocytic cells in the absence of added myeloid differentiation factors. NAM did not affect the expression the of cell surface granulocyte marker GR1 but led to a strong downregulation of MHC-II molecules. Taken together our data show that NAM induces a differentiation program in hematopoietic progenitors prompting them to undergo differentiation along the granulocyte path without reaching the status of fully developed granulocytes.

烟酰胺 (NAM) 是维生素 B3 的一种形式，是 NAD 的重要前体。这种二核苷酸（吡啶核苷酸）参与基本过程的调节，包括转录、细胞周期进程和 DNA 修复。在这里，我们评估了 NAM 对 IL-3 依赖性多能造血祖细胞系 FDCP-Mix 骨髓分化的影响。我们发现 NAM 降低了 pSTAT5 信号响应、细胞周期和自我更新潜力。它启动了一个非典型的髓样分化程序，导致粒细胞在没有添加髓样分化因子的情况下出现。NAM 不影响细胞表面粒细胞标志物 GR1 的表达，但导致 MHC-II 分子的强烈下调。