ESTROGEN INCREASES HIP-70 PLC-ALPHA MESSENGER-RIBONUCLEIC-ACID IN THERAT UTERUS AND HYPOTHALAMUS/

Citation
Mg. Kaplitt et al., ESTROGEN INCREASES HIP-70 PLC-ALPHA MESSENGER-RIBONUCLEIC-ACID IN THERAT UTERUS AND HYPOTHALAMUS/, Endocrinology, 133(1), 1993, pp. 99-104
Citations number
23
Categorie Soggetti
Endocrynology & Metabolism
Journal title
ISSN journal
00137227
Volume
133
Issue
1
Year of publication
1993
Pages
99 - 104
Database
ISI
SICI code
0013-7227(1993)133:1<99:EIHPMI>2.0.ZU;2-C
Abstract
In the ventromedial hypothalamus (VMH) of female rats, estrogen induce s a protein isoform, HIP-70, whose sequence is identical to a protein reported to be phosphoinositol-specific phospholipase-C-alpha (PLC-alp ha). Since previous studies explored induction only at the protein lev el, we examined both the distribution of HIP-70/PLC-alpha mRNA in vari ous tissues and the effects of estrogen on HIP-70/PLC-alpha mRNA. Usin g slot blot analysis, we found that HIP-70/PLC-alpha mRNA is most abun dant 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-7 0/PLC-alpha mRNA in these areas. Levels of HIP-70/PLC-alpha mRNA incre ased 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 es trogen 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 est rogen does increase HIP-70/PLC-alpha mRNA levels in certain tissues. S ince the induction of HIP-70/PLC-alpha mRNA in VMH is relatively modes t compared to the much larger induction of the HIP-70 protein isoform, regulation of HIP-70/PLC-alpha may entail both pre- and posttranslati onal mechanisms. Because members of the PLC family catalyze the hydrol ysis of phosphatidyl inositol, potentially activating several secondar y mediators (intracellular Ca2+, protein kinase-C, and eicanosoids), t his second messenger pathway may mediate some effects of estrogen.