Coordinate developmental regulation of purine catabolic enzyme expression in gastrointestinal and postimplantation reproductive tracts.
Coordinate developmental regulation of purine catabolic enzyme expression in gastrointestinal and postimplantation reproductive tracts.
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DOI：
10.1083/jcb.115.1.179
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发表时间：
1991-10
期刊：
影响因子：
--
通讯作者：
Aronow BJ
中科院分区：
文献类型：
--
作者：
Witte DP;Wiginton DA;Hutton JJ;Aronow BJ
使用组织化学检测，我们原位可视化了嘌呤核苷酸降解的完整代谢途径。从舌头到回肠，小鼠胃肠道 (GI) 管腔内衬的不同上皮细胞类型强烈共表达五种关键嘌呤分解代谢酶中的每一种。在出生后胃肠道的成熟过程中，每种酶的表达急剧增加。使用原位杂交，仅在经历有丝分裂后分化的胃肠道上皮细胞中检测到腺苷脱氨酶 (ADA) mRNA 的大量积累。以类似的方式，在发育中的母胎界面处，嘌呤分解代谢途径的高水平表达也发生在母体蜕膜细胞的独特亚群中，之前已知其表达高水平的碱性磷酸酶和 ADA。这种诱导几乎在植入后立即发生在胚周母体蜕膜细胞中，随后不久在抗胎期蜕膜细胞中发生，随后在胎盘蜕膜基底细胞中发生：所有这些细胞都含有被认为正在经历程序性细胞死亡的细胞类型。该途径在胚胎植入部位的表达似乎至关重要，因为已发现其在妊娠期间的药理学抑制具有胚胎致死或致畸作用。这些营养界面（胎盘和胃肠道）的嘌呤破坏似乎超越了嘌呤回收的任何潜在经济性，并且可能代表了对饮食消化或广泛的程序性细胞死亡背景下发生的核酸分解的生化适应。
Using histochemical detection, we have visualized in situ the complete metabolic pathway for the degradation of purine nucleotides. From the tongue to the ileum, diverse epithelial cell types lining the lumen of the mouse gastrointestinal (GI) tract strongly coexpress each of the five key purine catabolic enzymes. Dramatic increases in the expression of each enzyme occurred during postnatal maturation of the GI tract. Using in situ hybridization, an intense accumulation of adenosine deaminase (ADA) mRNA was detected only within GI epithelial cells undergoing postmitotic differentiation. In a similar manner, at the developing maternal-fetal interface, high level expression of the purine catabolic pathway also occurred in a unique subset of maternal decidual cells previously known to express high levels of alkaline phosphatase and ADA. This induction occurred almost immediately after implantation in the periembryonic maternal decidual cells, shortly thereafter in antimesometrial decidual cells, and later in cells of the placental decidua basalis: all of which contain cell types thought to be undergoing programmed cell death. The expression of the pathway at the site of embryo implantation appears to be critical because its pharmacologic inhibition during pregnancy has been found to be embryolethal or teratogenic. Purine destruction at these nutritional interfaces (placenta and gastrointestinal tract) seem to override any potential economy of purine salvage, and may represent biochemical adaptation to nucleic acid breakdown occurring in the context of dietary digestion or extensive programmed cell death.