Why the study?
Although 16 K PRL-induced mal-angiogenesis contributes to peripartum cardiomyopathy pathogenesis, the effect of full-length prolactin (23 K PRL) is poorly understood.
Does 23 K PRL-mediated PERK signaling protect against peripartum cardiomyopathy in mice?
Does 23 K PRL-mediated PERK signaling protect against peripartum cardiomyopathy in mice?
The interaction between full-length prolactin (23 K PRL) and PERK signaling provides cardioprotection during the peripartum period, suggesting a novel mechanistic pathway in peripartum cardiomyopathy.
Peripartum cardiomyopathy (PPCM) is a life-threatening heart failure occurring in the peripartum period. Although mal-angiogenesis, induced by the 16-kDa N-terminal prolactin fragment (16 K PRL), is involved in the pathogenesis, the effect of full-length prolactin (23 K PRL) is poorly understood. We transfected neonate rat cardiomyocytes with plasmids containing 23 K PRL or 16 K PRL in vitro and found that 23 K PRL, but not 16 K PRL, upregulated protein kinase RNA-like endoplasmic reticulum kinase (PERK) signaling, and hypoxia promoted this effect. During the perinatal period, cardiomyocyte-specific PERK homogenous knockout (CM-KO) mice showed PPCM phenotypes after consecutive deliveries. Downregulation of PERK or JAK/STAT signaling and upregulation of apoptosis were observed in CM-KO mouse hearts. Moreover, in bromocriptine-treated CM-KO mice, cardiac function did not improve and cardiomyocyte apoptosis was not suppressed during the peripartum period. These results demonstrate that interaction between 23 K PRL and PERK signaling is cardioprotective during the peripartum term.
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Shimizu et al. (2021) studied this question.
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