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• W2034652023 abstract "Objectives Prolactin (PRL) is a multifunctional hormone that influences multiple physiological processes. It has been shown to have a protective effect on the cardiovascular system; however, the mechanisms of this effect are poorly understood. The purpose of the study was to elucidate the role of PRL in intermittent hypoxia (IH)-induced apoptosis in the cardiovascular system. Method and results We established a hyperprolactinemic rat model by implanting two anterior pituitary (AP) glands into the renal capsule of male Sprague–Dawley rats. The rats were kept under normoxic conditions for 4 weeks after implantation in order to reach the expression plateau of PRL in the plasma, and then treated with IH for 7 or 14 days. Their hearts were then removed for histological and protein expression analyses. Cerebral cortex (CX)-grafted control rats challenged with IH displayed unique phenotypes such as a thicker heart wall, an abnormal myocardial architecture and an increased interstitial space of the left ventricle. They exhibited reduced expressions of p-JAK2, p-STAT5, cell cycle-dependent proteins (cyclin D1, cyclin E and cyclin A), IGF-IRα, PI3Kα, p-AKT and p-ERK1/2 in cardiomyocytes at 7 days. Conclusions Our comprehensive analysis suggested that high plasma PRL can protect rat cardiomyocytes against IH through (1) the p-JAK2 and p-STAT5 pathways for transient cell proliferation, (2) the PI3Kα/AKT and MAPK survival pathways through IGF-I, and (3) the downregulation of IGF-II and ERK5, which inhibit cell hypertrophy." @default.
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• W2034652023 date "2015-02-01" @default.
• W2034652023 modified "2023-10-18" @default.
• W2034652023 title "Prolactin protects cardiomyocytes against intermittent hypoxia-induced cell damage by the modulation of signaling pathways related to cardiac hypertrophy and proliferation" @default.
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• W2034652023 doi "https://doi.org/10.1016/j.ijcard.2014.11.154" @default.
• W2034652023 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/25531577" @default.
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