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Pericytes promote recovery from acute cardiac injury, but influence of early life stress (ELS) on pericyte maturation is unclear. We used immortalized cell models and global cohorts of mice with and without ELS to characterize interindividual variation in pericyte transcriptional response to cardiac injury and determine the effects of ELS on pericyte resilience. Murine adventitial pericytes responded to injury with co-upregulation of markers of maturation, as well as tissue regeneration and extracellular matrix remodeling. mT/mG reporter mice revealed that proliferating (Ki67+), mature (NG2+) pericytes were the most responsive to injury. Interestingly, pericytes from adult mice exposed to ELS displayed lower proliferative capacity and increased susceptibility to apoptosis after injury. ELS also modulated survival of mature pericytes, leading to reduced accumulation of NG2+ pericytes after injury, regardless of the sex or strain of mice. In addition, ELS resulted in decreased expression of several genes in ischemic pericytes, including those involved in stem cell and endothelial cell proliferation, and decreased proliferative capacity, indicating reduction in their regenerative capacity. Transcriptional analysis of pericytes from human subject cohorts revealed co-expression of NG2 and CD146 as markers of their maturation, and higher expression of the pro-apoptotic protein BAD and of some early markers of apoptosis in pericytes from patients with hypertension and ischemic heart disease. Our results demonstrate that pericytes are targets of ELS and susceptible to apoptosis. Furthermore, the co-expression of pericyte markers may serve as a prognostic marker of their maturation.Exactly? Rather than
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