Abstract
Preterm babies are at risk for lifelong abnormalities in cardiovascular and respiratory systems. The mechanisms and interventions to correct these abnormalities are unknown. Hypoxia is common during the neonatal period in these infants. The acute effects of hypoxia early in life could produce epigenetic programming resulting in long term effects. We studied the acute and long term effects of neonatal hypoxia (Hx, 12% O2) during postnatal days 2 to 20. Acutely, hypoxia severely reduced somatic growth, but produced cardiac right ventricular (RV) hypertrophy that persisted into adulthood (65 days old). The RV of adult Hx rats had higher content of contractile proteins and DNA. At 21 days, the expression of miR‐1 and miR‐206 was significantly downregulated in the RV of Hx rats. The growth of skeletal muscle was disproportionately depressed in Hx rats at 21 days but recovered after 45 days of normoxia. At 21 days the expression of miR‐1 and miR‐206 in skeletal muscle, was upregulated (~2 fold) while miR‐133a was downregulated (~22%). At 65 days of age the expression of miR‐1 remained elevated in the skeletal muscle of male Hx rats. These results indicate that microRNAs participate in reprogramming adaptations to a neonatal hypoxic episode in the heart and skeletal muscles of rats that can persist into adulthood. Supported by NIH Grants P01HD048721 and UL1RR031985.
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