Premium
Prolactin specifically increases pyruvate dehydrogenase Elα in rat lateral prostate epithelial cells
Author(s) -
Costello L. C.,
Liu Y.,
Franklin R. B.
Publication year - 1995
Publication title -
the prostate
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.295
H-Index - 123
eISSN - 1097-0045
pISSN - 0270-4137
DOI - 10.1002/pros.2990260404
Subject(s) - prostate , prolactin , biology , endocrinology , lactate dehydrogenase , epithelium , medicine , pathology , enzyme , hormone , cancer , biochemistry
Prolactin is an important regulator of prostate citrate production. In rats this regulatory effect of prolactin is specific for lateral prostate, and has no effect on either ventral or dorsal prostate. The mechanisms by which prolactin regulates prostate citrate production have not been elucidated. Two key regulatory enzymes involved in citrate synthesis by prostate epithelial cells are mitochondrial aspartate aminotransferase (mAAT) which provides oxalacetate, and PDH E1α (pyruvate dehydrogenase) which provides acetyl CoA for citrate synthesis. Our previous studies demonstrated that prolactin regulates mAAT. However, an increase in citrate synthesis would require an increase in both oxalacetate and acetyl CoA. Therefore, we investigated the possibility that prolactin might also regulate PDH E1α in LP epithelial cells. The present studies demonstrate that prolactin administration (1 mg/rat) to rats resulted in an increased level of E1α in LP epithelial cells within 6 hr, but had no effect on the E1α level of VP epithelial cells. In vitro studies demonstrated that exposure of freshly prepared LP epithelial cells to prolactin (0.1–1.0 μg/ml) resulted in increased levels of E1α. Prolactin had no effect on either VP or DP epithelial cells. The stimulatory effect of prolactin on E1α was inhibited by actinomycin and cycloheximide, thereby indicating that prolactin stimulated the biosynthesis of E1α. The studies reveal that prolactin specifically stimulates E1α levels of LP epithelial cells, whereas testosterone specifically stimulates E1α levels of VP epithelial cells. At this time, we propose that the effects of prolactin and testosterone involve increased expression of the E1α gene of LP and VP epithelial cells, respectively.