Abstract. Retinoic acid (RA) plays a critical role in cell growth and tissue development. RA is also a regulating factor of pituitary function. RA is synthesized from retinoids through oxidation processes. The oxidation of retinal to RA is catalyzed by the retinaldehyde dehydrogenases (RALDHs), including RALDH1, RALDH2 and RALDH3. Recently, we demonstrated that RALDH1 is expressed in the anterior pituitary glands of adult male rats. However, the expression of RALDH1 in the female pituitary gland and the regulation of RALDH1 expression have not been determined. Therefore, we examined the expression of RALDH1 mRNA in the pituitary glands of adult female rats. By in situ hybridization with digoxigenin-labeled cRNA probes and quantitative real-time PCR analysis, we found that the expression level of RALDH1 was significantly lower in estrus as compared to proestrus, metestrus and diestrus. RALDH1 mRNA levels increased after ovariectomy and decreased remarkably after a 1-week treatment with 17β-estradiol implants. Estradiol (0.01-100 µg per rat) dose-dependently decreased the expression of RALDH1 in the pituitary glands after 24 hours of subcutaneous administration. These results clearly show that RALDH1 mRNA expression is suppressed by estrogen. We speculate that the generation of RA is regulated by estrogen and that RA plays a role in the estrus cycle through paracrine and/or autocrine mechanisms in the anterior pituitary gland of female rats.
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.
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