Estrogen increases HIP-70/PLC-alpha messenger ribonucleic acid in the rat uterus and hypothalamus.
| Publication Type | Academic Article |
| Authors | Kaplitt M, Kleopoulos S, Pfaff D, Mobbs C |
| Journal | Endocrinology |
| Volume | 133 |
| Issue | 1 |
| Pagination | 99-104 |
| Date Published | 07/01/1993 |
| ISSN | 0013-7227 |
| Keywords | Estradiol, Hypothalamus, Isoenzymes, RNA, Messenger, Type C Phospholipases, Uterus |
| Abstract | 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-alpha (PLC-alpha). Since previous studies explored induction only at the protein level, we examined both the distribution of HIP-70/PLC-alpha mRNA in various tissues and the effects of estrogen on HIP-70/PLC-alpha mRNA. Using slot blot analysis, we found that HIP-70/PLC-alpha 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-alpha mRNA in these areas. Levels of HIP-70/PLC-alpha mRNA increased greater than 3-fold in the uterus 18 h after estrogen treatment. HIP-70/PLC-alpha 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-alpha mRNA. These results indicate that estrogen does increase HIP-70/PLC-alpha mRNA levels in certain tissues. Since the induction of HIP-70/PLC-alpha mRNA in VMH is relatively modest compared to the much larger induction of the HIP-70 protein isoform, regulation of HIP-70/PLC-alpha 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. |
| DOI | 10.1210/endo.133.1.8319593 |
| PubMed ID | 8319593 |