Department of Inflammation and Immunity, Lerner Research Institute, The Cleveland Clinic, Cleveland, OH 44195, USA.
Cells. 2022 Sep 12;11(18):2838. doi: 10.3390/cells11182838.
Ever since the days of NO being proclaimed as the "molecule of the year", the molecular effects of this miracle gas on the globins have remained elusive. While its vasodilatory role in the cardiopulmonary system and the vasculature is well recognized, the molecular underpinnings of the NO-globin axis are incompletely understood. We show, by transwell co-culture of nitric oxide (NO) generating, HEK eNOS/nNOS cells, and K562 erythroid or C2C12 muscle myoblasts, that low doses of NO can effectively insert heme into hemoglobin (Hb) and myoglobin (Mb), making NO not only a vasodilator, but also a globin heme trigger. We found this process to be dependent on the NO flux, occurring at low NO doses and fading at higher doses. This NO-triggered heme insertion occurred into Hb in just 30 min in K562 cells and into muscle Mb in C2C12 myoblasts between 30 min and 1 h, suggesting that the classical effect of NO on upregulation of globin (Hb or Mb) is just not transcriptional, but may involve sufficient translational events where NO can cause heme-downloading into the apo-globins (Hb/Mb). This effect of NO is unexpected and highlights its significance in maintaining globins in its heme-containing holo-form, where such heme insertions might be required in the circulating blood or in the muscle cells to perform spontaneous functions.
自从一氧化氮(NO)被宣布为“年度分子”以来,这种神奇气体对球蛋白的分子效应仍然难以捉摸。虽然其在心肺系统和脉管系统中的血管扩张作用已得到充分认识,但 NO-球蛋白轴的分子基础仍不完全清楚。我们通过共培养产生一氧化氮(NO)的 HEK eNOS/nNOS 细胞,与 K562 红细胞或 C2C12 肌肉成肌细胞,证明低剂量的 NO 可以有效地将血红素插入血红蛋白(Hb)和肌红蛋白(Mb)中,使 NO 不仅是一种血管扩张剂,还是一种球蛋白血红素触发剂。我们发现这个过程依赖于 NO 通量,在低 NO 剂量下发生,在高剂量下消失。在 K562 细胞中,这个 NO 触发的血红素插入过程仅需 30 分钟即可完成,而在 C2C12 成肌细胞中,插入肌红蛋白需要 30 分钟至 1 小时,这表明 NO 对球蛋白(Hb 或 Mb)上调的经典作用不仅仅是转录的,而是可能涉及足够的翻译事件,在这些事件中,NO 可以导致血红素进入脱辅基球蛋白(Hb/Mb)。NO 的这种作用是出乎意料的,突出了其在维持球蛋白处于血红素结合的全氧形式中的重要性,在这种形式中,在循环血液或肌肉细胞中可能需要进行这种血红素插入,以发挥自发功能。