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Wnt4 的表达受雌激素调控,通过雌激素受体 α 依赖途径在大鼠垂体生长激素分泌细胞中。

The expression of Wnt4 is regulated by estrogen via an estrogen receptor alpha-dependent pathway in rat pituitary growth hormone-producing cells.

机构信息

Department of Pathology, Tokai University School of Medicine, 143 Shimokasuya, Isehara, Kanagawa 259-1193, Japan.

出版信息

Acta Histochem Cytochem. 2009 Dec 29;42(6):205-13. doi: 10.1267/ahc.09033. Epub 2009 Dec 22.

DOI:10.1267/ahc.09033
PMID:20126574
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2808504/
Abstract

Wnt signaling is important in many aspects of cell biology and development. In the mouse female reproductive tract, Wnt4, Wnt5a, and Wnt7a show differential expression during the estrus cycle, suggesting that they participate in female reproductive physiology. Although the pituitary is a major gland regulating reproduction, the molecular mechanism of Wnt signaling here is unclear. We elucidated the subcellular distribution of Wnt4 in the pituitary of estrogen-treated ovariectomized female rats. Expression of Wnt4 mRNA increased dramatically, particularly in proestrus compared with estrus and metestrus. Wnt4 protein was observed in the cytoplasm of almost all growth hormone (GH)-producing cells and in only a few thyroid-stimulating hormone beta (TSHbeta)-producing cells. In rat GH-producing pituitary tumor (MtT/S) cells, estrogen-induced expression of Wnt4 mRNA was completely inhibited by estrogen receptor antagonist ICI 182,780 in vitro. Thus, rat pituitary GH cells synthesize Wnt4 and this is induced by estrogen mediated via an estrogen receptor alpha-dependent pathway.

摘要

Wnt 信号通路在细胞生物学和发育的许多方面都很重要。在雌性小鼠生殖道中,Wnt4、Wnt5a 和 Wnt7a 在发情周期中表现出不同的表达,表明它们参与了雌性生殖生理学。尽管垂体是调节生殖的主要腺体,但这里的 Wnt 信号通路的分子机制尚不清楚。我们阐明了雌激素处理去卵巢雌性大鼠垂体中 Wnt4 的亚细胞分布。Wnt4 mRNA 的表达显著增加,特别是在发情前期与发情期和间情期相比。Wnt4 蛋白存在于几乎所有生长激素 (GH) 产生细胞的细胞质中,而仅存在于少数促甲状腺激素 β (TSHβ) 产生细胞中。在大鼠 GH 产生垂体瘤 (MtT/S) 细胞中,体外雌激素受体拮抗剂 ICI 182,780 完全抑制了雌激素诱导的 Wnt4 mRNA 的表达。因此,大鼠垂体 GH 细胞合成 Wnt4,并且这种合成是由雌激素通过雌激素受体 α 依赖性途径介导的。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/341c/2808504/bd913e5cf02c/AHC09033f08.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/341c/2808504/fdf329c736a7/AHC09033f01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/341c/2808504/ca24f2dd7920/AHC09033f02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/341c/2808504/46c6b86faeb3/AHC09033f03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/341c/2808504/517f00e53943/AHC09033f04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/341c/2808504/f8ddd686732c/AHC09033f05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/341c/2808504/2b5f9e905b09/AHC09033f06.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/341c/2808504/9eb0c2b73383/AHC09033f07.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/341c/2808504/bd913e5cf02c/AHC09033f08.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/341c/2808504/fdf329c736a7/AHC09033f01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/341c/2808504/ca24f2dd7920/AHC09033f02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/341c/2808504/46c6b86faeb3/AHC09033f03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/341c/2808504/517f00e53943/AHC09033f04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/341c/2808504/f8ddd686732c/AHC09033f05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/341c/2808504/2b5f9e905b09/AHC09033f06.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/341c/2808504/9eb0c2b73383/AHC09033f07.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/341c/2808504/bd913e5cf02c/AHC09033f08.jpg

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