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
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.