Abstract: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 regula… Show more
“…In previous studies, we reported that RA-synthesizing enzyme, retinaldehyde dehydrogenase 1, was expressed in folliculostellate cells and lactotrophs but not in somatotrophs [22,23]. In the present study, we found that RA increased Ghrh-r and Ghs-r gene expression and promoted GHRH-and ghrelin-induced GH release from isolated rat anterior pituitary cells.…”
“…In previous studies, we reported that RA-synthesizing enzyme, retinaldehyde dehydrogenase 1, was expressed in folliculostellate cells and lactotrophs but not in somatotrophs [22,23]. In the present study, we found that RA increased Ghrh-r and Ghs-r gene expression and promoted GHRH-and ghrelin-induced GH release from isolated rat anterior pituitary cells.…”
“…For normalization, we also quantified β-actin using forward (5'-tGG CAC CAC ACt ttC tAC AAt GAG C-3') and reverse (5'-GGG tCA tCt ttt CAC GGt tGG-3') primers. gland of female rats [19]. our in vivo study indicated that estrogen is a candidate for regulator of RALdh1 expression in the pituitary, but the mechanisms that may be responsible for this effect are not understood.…”
Section: Quantification Of Raldh1 Mrna Levels By Real-time Reverse Trmentioning
confidence: 78%
“…this decrease in RALdh1 expression was observed in cells incubated with a 17β-estradiol concentration as low as 1 x 10 -14 M. Lieberman et al [29] reported a dose-dependent increase in prolactin synthesis at physiological concentrations of estradiol (1 x 10 -11 -1 x 10 -6 M) in a rat pituitary cell culture. We previously reported that RALdh1 mRnA expression in the pituitary gland of ovariectomized rats was suppressed after a single subcutaneous injection of 17β-estradiol: mRnA expression in response to 0.01, 0.1, 1, 10, and 100 μg of 17β-estradiol decreased by 13%, our recent work has shown that RALdh1 mRnA expression level in the pituitary gland is lower in female than in male rats [19]. Moreover, we observed that RALdh1 mRnA expression was lower in female rats treated with 17β-estradiol [19].…”
Section: Treatment With Er Antagonist and Agonistsmentioning
confidence: 88%
“…We previously reported that RALdh1 mRnA expression in the pituitary gland of ovariectomized rats was suppressed after a single subcutaneous injection of 17β-estradiol: mRnA expression in response to 0.01, 0.1, 1, 10, and 100 μg of 17β-estradiol decreased by 13%, our recent work has shown that RALdh1 mRnA expression level in the pituitary gland is lower in female than in male rats [19]. Moreover, we observed that RALdh1 mRnA expression was lower in female rats treated with 17β-estradiol [19]. In the present study, we confirmed that both RALDH1 mRNA transcription and protein production in the pituitary gland were lower after implantation of a 17β-estradiol-filled tube in male rats ( Fig.…”
Section: Treatment With Er Antagonist and Agonistsmentioning
Abstract. Retinoic acid (RA) plays a critical role in embryonic development, growth, and reproduction. RA is synthesized from retinoids via oxidation processes, and the oxidation of retinal to RA is catalyzed by the retinaldehyde dehydrogenases (RALdhs). We previously reported that RALdh1 mRnA was expressed in the anterior pituitary glands of adult rats and suppressed by administration of 17β-estradiol in vivo. however, little is known about the mechanism regulating pituitary RALdh1 expression. In order to characterize the mechanism of estrogen-induced RALdh1 reduction, we examined the effect of 17β-estradiol on the regulation of pituitary RALDH1 gene expression and protein production both in vivo and in vitro. Using quantitative real-time PCR and immunoblot analysis, we found that levels of RALdh1 gene expression and protein production markedly decreased after 1-week treatment with 17β-estradiol in male rats. In immunohistochemical analysis, RALDH1-immunoreaction was observed in prolactin cells and folliculo-stellate cells. In 17β-estradiol-treated rats, RALdh1-immunoreactivity was lower in prolactin cells, but not in folliculo-stellate cells. treatment of isolated anterior pituitary cells with 17β-estradiol (10 -14 -10 -8 M) decreased expression of RALdh1 mRnA in a dose-dependent manner. estradiol-induced suppression of RALdh1 expression was completely blocked by the estrogen receptor (eR) antagonist ICI 182, 780. The ERα-selective agonist propylpyrazole triol (10 -8 M) mimicked the effect of 17β-estradiol on RALDH1 expression, but the ERβ-selective agonist diarylpropionitrile (10 -8 M) did not. these results strongly suggest that RALDH1 mRNA expression is suppressed by 17β-estradiol through ERα, and that estrogen regulates the expression of RALdh1 and production of RA in the anterior pituitary gland.
“…In situ hybridization was performed with digoxigenin (DIG)-labeled cRNA probes, as described in our previous report [9]. Antisense and sense cRNA probes of rat MK were synthesized by in vitro transcription with DIG RNA Labeling Mix (Roche Diagnostics, Penzberg, Germany) [10].…”
Section: In Situ Hybridization and Immunohistochemistrymentioning
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.