N-glycomic of mouse hearts post myocardial infarction

The neonatal mammalian heart is capable of scarless regeneration after injury but this potency is lost shortly after birth. Recent studies have suggested that metabolic and immune cell changes that occur during the neonatal time window antagonize regenerative potency, yet the molecular trigger that orchestrates these events remains largely unknown. Here, we investigated whether changes in glycosylation, which are known to alter cytokine signaling, might direct the transition from regenerative to non-regenerative state during the first week after birth in the mouse. Most glycan structures were unchanged during this time with the notable exception of terminal sialylation, resulting in a shift from nearly exclusively α2,3-linked sialic acid (SA) after injury at postnatal day 1 (P1) to abundant α2,6-linked SA a week later (P7). Our data indicate that the change in sialyl linkage triggers the transition from a regenerative state at P1 to a non-regenerative but anti-apoptotic response to injury by P7.新生哺乳动物心脏在损伤后具备无瘢痕再生能力，但该再生潜能于出生后不久便会丧失。近期研究表明，新生阶段发生的代谢与免疫细胞变化会拮抗再生潜能，但调控上述过程的分子触发因素仍未完全明确。本研究探讨了已知可改变细胞因子信号转导的糖基化（glycosylation）变化，是否会介导小鼠出生后第一周内从再生状态向非再生状态的转变。在此期间，绝大多数糖链结构未发生显著变化，仅末端唾液酸化修饰存在显著差异：小鼠出生后第1天（P1）发生损伤时，心脏几乎仅表达α2,3-连接唾液酸（SA）；而一周后的第7天（P7），则出现大量α2,6-连接唾液酸。我们的数据表明，唾液酸连接方式的改变，会促使小鼠心脏在P1时的再生状态，转变为P7时对损伤产生的非再生但抗凋亡应答。