title: Reduction of retinaldehyde dehydrogenase 1 expression and production in estrogen-induced prolactinoma of rat.
abstract: Retinoic acid (RA) plays a critical role in normal development and tissue maintenance and is also a regulatory factor of anterior pituitary cells. We previously demonstrated that a retinoic acid-synthesizing enzyme, retinaldehyde dehydrogenase 1 (RALDH1), is expressed in prolactin cells of adult rats and that estrogen suppressed RALDH1 expression. It is suggested that RA plays a role as a paracrine and/or autocrine signaling molecule in the anterior pituitary gland. However, the presence of RALDH1 in pituitary tumors has not been demonstrated. In this study, we examined the expression of RALDH1 in diethylstilbestrol-induced prolactinoma of LEXF RI rats. Quantitative analysis of mRNA levels by real-time PCR demonstrated drastic reduction of RALDH1 expression in the prolactinoma. We have also detected both mRNA expression and production by in situ hybridization and immunohistochemistry. Both mRNA-expressing cells and immunopositive cells remarkably decreased after 4 weeks of treatment with diethylstilbestrol. Fluorescence double immunohistochemistry of RALDH1 and prolactin revealed that prolactin-immunopositive cells do not colocalize with RALDH1 in the prolactinoma. These results suggest that the reduction of local RA generation relates to cell proliferation and tumorigenesis of lactotrophs.
authors.affiliation: Division of Histology and Cell Biology, Department of Anatomy, Jichi Medical University School of Medicine, 3311-1 Yakushiji, Shimotsuke, Tochigi 329-0498, Japan.
authors.forename: Ken
authors.initials: K
authors.lastname: Fujiwara
authors.forename: Bulgan
authors.initials: B
authors.lastname: Davaadash
authors.forename: Megumi
authors.initials: M
authors.lastname: Yatabe
authors.forename: Motoshi
authors.initials: M
authors.lastname: Kikuchi
authors.forename: Kotaro
authors.initials: K
authors.lastname: Horiguchi
authors.forename: Kenji
authors.initials: K
authors.lastname: Kusumoto
authors.forename: Tom
authors.initials: T
authors.lastname: Kouki
authors.forename: Takashi
authors.initials: T
authors.lastname: Yashiro
mesh_terms: D000080924:Aldehyde Dehydrogenase 1 Family; D000818:Animals; D000970:Antineoplastic Agents / Q000378:metabolism; D004054:Diethylstilbestrol / Q000494:pharmacology; D004968:Estrogens, Non-Steroidal / Q000494:pharmacology*; D005260:Female; D006801:Humans; D010911:Pituitary Neoplasms / Q000139:chemically induced / Q000201:enzymology* / Q000473:pathology; D011388:Prolactin / Q000378:metabolism; D015175:Prolactinoma / Q000139:chemically induced / Q000201:enzymology* / Q000473:pathology; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D050697:Retinal Dehydrogenase / Q000235:genetics / Q000378:metabolism*; D014212:Tretinoin / Q000378:metabolism
chemical_list: D000970:Antineoplastic Agents; D004968:Estrogens, Non-Steroidal; D012333:RNA, Messenger; D014212:Tretinoin; D004054:Diethylstilbestrol; D011388:Prolactin; D000080924:Aldehyde Dehydrogenase 1 Family; C523119:Aldh1a1 protein, rat; D050697:Retinal Dehydrogenase