Effects of transforming growth factor beta-1 and all-trans-retinoic acid on androgen-induced development of neonatal mouse bulbourethral glands in vitro.
Effects of transforming growth factor beta-1 and all-trans-retinoic acid on androgen-induced development of neonatal mouse bulbourethral glands in vitro.
复制标题
转化生长因子β-1和全反式视黄酸对雄激素诱导的新生小鼠尿道球腺体外发育的影响。
DOI：
10.1046/j.1365-2605.2000.00209.x
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发表时间：
2000
影响因子：
--
通讯作者：
Cunha,GR
中科院分区：
文献类型：
--
作者：
Tanji,N;Rahman,SA;Terada,N;Yokoyama,M;Cunha,GR
体外研究了转化生长因子 β-1 (TGF-β1) 和全反式维甲酸 (All-trans-RA) 对新生小鼠尿道球腺 (BUG) 发育的影响。将来自 0 日龄雄性小鼠的 BUG 在含有转铁蛋白和牛血清白蛋白的无血清、化学成分确定的培养基中培养 6 天，并单独或联合补充 5α-二氢睾酮 (DHT；10–8M) 和胰岛素 (10μg/mL)。培养前，0 日龄小鼠的 BUG 由间充质包裹的简单上皮雏形组成。在含有 DHT 和胰岛素或单独 DHT 的培养基中培养的 BUG 发生上皮生长和导管分支，但在单独存在胰岛素的情况下培养的 BUG 中不发生上皮分支。在含有胰岛素和 DHT 的培养基中添加浓度 > 5 ng/mL (0.2 × 10-9M) 的 TGF-β1，以剂量依赖性方式抑制了 BUG 总体大小、上皮面积和导管分支的预期增加。 TGF-β1 还降低上皮和间质的 [3H]-胸苷标记指数。 10 ng/mL 的 TGF-β1 对在单独含有 DHT 的培养基中培养的 BUG 产生了这些抑制作用。在含有 DHT 加胰岛素的培养基中添加全反式 RA（10-8 至 10-6M），或单独添加 DHT 不会对 BUG 的整体大小或上皮生长和导管分支产生显着影响。 10-6M 的全反式 RA 降低了在 DHT 加胰岛素或单独 DHT 培养基中培养的 BUG 间充质的 [3H]-胸苷标记指数，但不降低上皮的 [3H]-胸苷标记指数。目前的结果表明，TGF-β1 抑制雄激素诱导的上皮和间质生长以及新生小鼠 BUG 的上皮形态发生。生理浓度的 All-trans-RA 无法模拟 TGF-β1 的这种抑制作用。
Effects of transforming growth factor β‐1 (TGF‐β1) and all‐trans‐retinoic acid (All‐trans‐RA) on development of bulbourethral glands (BUGs) of neonatal mice were investigated in vitro. BUGs from 0‐day‐old male mice were cultured for 6 days in serum‐free, chemically defined medium containing transferrin and bovine serum albumin, supplemented with 5α‐dihydrotestosterone (DHT; 10–8M) and insulin (10 μg/mL) alone or in combination. Prior to culture, BUGs from 0‐day‐old mice consisted of a simple epithelial rudiment encapsulated by mesenchyme. Epithelial growth and ductal branching occurred in BUGs cultured in medium containing DHT and insulin or DHT alone, but epithelial branching did not occur in BUGs cultured in the presence of insulin alone. Addition of TGF‐β1 at concentrations of > 5 ng/mL (0.2 × 10–9M) to medium containing both insulin and DHT, inhibited the expected increase in overall size of BUGs, epithelial area and ductal branching in a dose‐dependent manner. TGF‐β1 also decreased [3H]‐thymidine labelling indices of both epithelium and mesenchyme. TGF‐β1 at 10 ng/mL elicited these inhibitory effects on BUGs cultured in medium containing DHT alone. Addition of All‐trans‐RA (10–8to 10–6M) to the medium containing DHT plus insulin, or DHT alone did not exert significant effects on either overall size of BUGs or epithelial growth and ductal branching. All‐trans‐RA at 10–6M decreased the [3H]‐thymidine labelling index of mesenchyme of BUGs cultured in medium with DHT plus insulin or DHT alone, but did not decrease the [3H]‐thymidine labelling index of epithelium. The present results indicate that TGF‐β1 inhibits androgen‐induced epithelial and mesenchymal growth as well as epithelial morphogenesis of BUGs from neonatal mice. Such an inhibitory effect of TGF‐β1 is not mimicked by All‐trans‐RA at physiological concentrations.