Essential roles of epithelial bone morphogenetic protein signaling during prostatic development.
Essential roles of epithelial bone morphogenetic protein signaling during prostatic development.
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DOI：
10.1210/en.2013-2054
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发表时间：
2014-07
期刊：
影响因子：
4.8
通讯作者：
Yamada G
中科院分区：
文献类型：
--
作者：
Omori A;Miyagawa S;Ogino Y;Harada M;Ishii K;Sugimura Y;Ogino H;Nakagata N;Yamada G
前列腺是男性的性附属器官。前列腺上皮主要由基底细胞和腔细胞组成，它们是从胚胎期尿生殖窦上皮分化而来的。前列腺肿瘤被认为起源于基底细胞和腔细胞。然而，促进正常上皮分化的因素尚未得到很好的阐明，特别是骨形态发生蛋白（Bmp）信号传导。这项研究表明，BMP信号显着增加前列腺分化过程中的管腔上皮细胞，这是监测磷酸化Smad 1/5/8的表达。为了阐明前列腺发育过程中上皮分化的机制和BMP信号转导的功能，进行了上皮特异性BMP受体1a（Bmpr 1a）的条件性雄性突变小鼠分析。我们证明，BMP信号是不可缺少的管腔细胞成熟，调节基底细胞增殖。前列腺上皮调控基因Nkx3.1的表达在Bmpr 1a突变体中显著降低。这些结果表明，BMP信号是前列腺上皮分化的关键因素，可能通过控制前列腺调节基因Nkx3.1。
Prostate is a male sex-accessory organ. The prostatic epithelia consist primarily of basal and luminal cells that differentiate from embryonic urogenital sinus epithelia. Prostate tumors are believed to originate in the basal and luminal cells. However, factors that promote normal epithelial differentiation have not been well elucidated, particularly for bone morphogenetic protein (Bmp) signaling. This study shows that Bmp signaling prominently increases during prostatic differentiation in the luminal epithelia, which is monitored by the expression of phosphorylated Smad1/5/8. To elucidate the mechanism of epithelial differentiation and the function of Bmp signaling during prostatic development, conditional male mutant mouse analysis for the epithelial-specific Bmp receptor 1a (Bmpr1a) was performed. We demonstrate that Bmp signaling is indispensable for luminal cell maturation, which regulates basal cell proliferation. Expression of the prostatic epithelial regulatory gene Nkx3.1 was significantly reduced in the Bmpr1a mutants. These results indicate that Bmp signaling is a key factor for prostatic epithelial differentiation, possibly by controlling the prostatic regulatory gene Nkx3.1.
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影响因子：
3.2
作者：
Hudson, DL;Guy, AT;Masters, JRW
通讯作者：
Masters, JRW
DOI：
10.1006/bbrc.1997.7124
发表时间：
1997-08-28
影响因子：
3.1
作者：
Feil, R;Wagner, J;Chambon, P
通讯作者：
Chambon, P
影响因子：
2.7
作者：
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通讯作者：
de Caestecker, Mark
影响因子：
2.5
作者：
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通讯作者：
Bieberich, CJ
影响因子：
2.5
作者：
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通讯作者：
Shen, Michael M.