The analysis of epigenetic changes in GH-IGF-1 axis of small for gestational age rats

参与小胎龄（SGA）追赶生长的激素因素尚不清楚。为了揭示SGA生长衰竭的机制，我们分析了大鼠模型中的生长激素(GH)/胰岛素样生长因子(IGF)-1轴。SGA和非追赶型生长（SGA- ncg）大鼠肝生长激素受体（GHR）表达降低。我们发现GHR表达的降低是由SGA-NCG大鼠肝脏中miR-322表达的升高引起的。我们进一步发现，在SGA-NCG大鼠的肝脏中，miR-322编码区的DNA甲基化减少，并且GHR和miR-322表达的这些变化是跨代的。

The hormonal factors involved in catch-up growth in the small for gestational age (SGA) are unknown. To reveal the mechanism underlying growth failure in SGA, we analyzed growth hormone (GH)/ insulin-like growth factor (IGF)-1 axis in a rat model. In SGA and non-catch up growth (SGA-NCG) rats, hepatic growth hormone receptor (GHR) expression was reduced. We revealed that the reduction of GHR expression is caused by elevation of miR-322 expression in the liver of SGA-NCG rats. We further found that DNA methylation in the miR-322 coding region is reduced in the liver of SGA-NCG rats and thatthese changes in the expression of GHR and miR-322 are trans-generational.