Estrogen increases HIP-70/PLC-α messenger ribonucleic acid in the rat uterus and hypothalamus

In the ventromedial hypothalamus (VMH) of female rats, estrogen induces a protein isoform, HIP-70, whose sequence is identical to a protein reported to be phosphoinositol-specific phospholipase-C-α (PLC-α). Since previous studies explored induction only at the protein level, we examined both the distribution of HIP-70/PLC-α mRNA in various tissues and the effects of estrogen on HIP-70/PLC-α mRNA. Using slot blot analysis, we found that HIP-70/PLC-α mRNA is most abundant in pituitary, uterus, and VMH of female rats compared with other brain regions and tissues. Since these are target tissues for estrogen action, we examined the effects of estrogen on the abundance of HIP-70/PLC-α mRNA in these areas. Levels of HIP-70/PLC-α mRNA increased greater than 3-fold in the uterus 18 h after estrogen treatment. HIP-70/PLC-α mRNA in the VMH also increased about 35% 3 h after estrogen treatment. In situ hybridization corroborated the induction in the ventrolateral ventromedial hypothalamus. No effect of estrogen was observed on pituitary PLC-α mRNA. These results indicate that estrogen does increase HIP-70/PLC-α mRNA levels in certain tissues. Since the induction of HIP-70/PLC-α mRNA in VMH is relatively modest compared to the much larger induction of the HIP-70 protein isoform, regulation of HIP-70/PLC-α may entail both pre- and posttranslational mechanisms. Because members of the PLC family catalyze the hydrolysis of phosphatidyl inositol, potentially activating several secondary mediators (intracellular Ca²⁺, protein kinase-C, and eicanosoids), this second messenger pathway may mediate some effects of estrogen.