Expression of retinaldehyde dehydrogenase (RALDH)2 and RALDH3 but not RALDH1 in the developing anterior pituitary glands of rats

Fujiwara, Ken; Maekawa, Fumihiko; Kikuchi, Motoshi; Takigami, Shu; Yada, Toshihiko; Yashiro, Takashi

doi:10.1007/s00441-006-0345-7

Cited by 41 publications

(36 citation statements)

References 24 publications

(19 reference statements)

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“…our previous work revealed that RALdh2 and RALdh3 mRnA were expressed in the embryonic pituitary gland of rat [17], whereas RALdh1 mRnA was expressed in the pituitary gland of adult rat [18]. We speculated that RA may play a role as an autocrine and/or paracrine signaling molecule in this gland.…”

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confidence: 90%

Estrogen Receptor Alpha Regulates Retinaldehyde Dehydrogenase 1 Expression in Rat Anterior Pituitary Cells

et al. 2009

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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.

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confidence: 90%

Estrogen Receptor Alpha Regulates Retinaldehyde Dehydrogenase 1 Expression in Rat Anterior Pituitary Cells

et al. 2009

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“…We previously reported that RALDH2 and RALDH3, but not RALDH1, are expressed in the embryonic anterior pituitary gland of the rat [3]. We recently also reported that RALDH1 mRNA, but not RALDH2 or RALDH3 mRNA, is expressed in the anterior pituitary gland of adult rats [4].…”

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confidence: 93%

Estrogen Suppresses Retinaldehyde Dehydrogenase 1 Expression in the Anterior Pituitary Glands of Female Rats

Fujiwara

Davaadash²,

Kikuchi

et al. 2008

Endocr J

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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.

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“…The tissues were then embedded in Tissue-Tek OCT compound (Sakura Finetechnical, Tokyo, Japan), and frozen sections (8 µm) were obtained using a cryostat (CM3000, Leica Microsystems, Wetzlar, Germany). In situ hybridization was performed with digoxigenin (DIG)-labeled cRNA probes, as described in our previous report (Fujiwara et al 2007a). The following DNA fragments of rat TGFβ2 (NM_031131) and TGFβ receptor II (NM_031132) were amplified from rat pituitary cDNA by PCR (see Table 2 for primer information).…”

Section: In Situ Hybridizationmentioning

confidence: 99%

Folliculostellate cell interacts with pericyte via TGFβ2 in rat anterior pituitary

Tsukada¹,

Azuma²,

Horiguchi³

et al. 2016

Journal of Endocrinology

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The anterior pituitary gland comprises five types of endocrine cells plus non-endocrine cells including folliculostellate cells, endothelial cells, and capillary mural cells (pericytes). In addition to being controlled by the hypothalamic-pituitary-target organ axis, the functions of these cells are likely regulated by local cell and extracellular matrix (ECM) interactions. However, these complex interactions are not fully understood. We investigated folliculostellate cell-mediated cell-to-cell interaction. Using S100β-GFP transgenic rats, which express GFP in folliculostellate cells, we designed a three-dimensional cell culture to examine the effects of folliculostellate cells. Interestingly, removal of folliculostellate cells reduced collagen synthesis (Col1a1 and Col3a1). Because pericytes are important collagen-producing cells in the gland, we stained for desmin (a pericyte marker). Removal of folliculostellate cells resulted in fewer desmin-positive pericytes and less desmin mRNA. We then attempted to identify the factor mediating folliculostellate cell-pericyte interaction. RT-PCR and in situ hybridization revealed that the important profibrotic factor transforming growth factor beta-2 (TGFβ2) was specifically expressed in folliculostellate cells and that TGFβ receptor II was expressed in pericytes, endothelial cells, and parenchymal cells. Immunocytochemistry showed that TGFβ2 induced SMAD2 nuclear translocation in pericytes. TGFβ2 increased collagen synthesis in a dose-dependent manner. This action was completely blocked by TGFβ receptor I inhibitor (SB431542). Diminished collagen synthesis in folliculostellate cell-deficient cell aggregates was partially recovered by TGFβ2. TGFβ2-mediated folliculostellate cell-pericyte interaction appears to be essential for collagen synthesis in rat anterior pituitary. This finding sheds new light on local cell-ECM interactions in the gland. 159-170 229:2 FS cell interacts with pericyte via TGFβ2t tsukada and others

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Expression of retinaldehyde dehydrogenase (RALDH)2 and RALDH3 but not RALDH1 in the developing anterior pituitary glands of rats

Cited by 41 publications

References 24 publications

Estrogen Receptor Alpha Regulates Retinaldehyde Dehydrogenase 1 Expression in Rat Anterior Pituitary Cells

Estrogen Receptor Alpha Regulates Retinaldehyde Dehydrogenase 1 Expression in Rat Anterior Pituitary Cells

Estrogen Suppresses Retinaldehyde Dehydrogenase 1 Expression in the Anterior Pituitary Glands of Female Rats

Folliculostellate cell interacts with pericyte via TGFβ2 in rat anterior pituitary

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