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.