RELAXATION OF IMPRINTING IN TROPHOBLASTIC DISEASE
RELAXATION OF IMPRINTING IN TROPHOBLASTIC DISEASE
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DOI：
10.1006/gyno.1994.1118
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发表时间：
1994-05-01
影响因子：
4.7
通讯作者：
HOCHBERG, A
中科院分区：
文献类型：
--
作者：
ARIEL, I;LUSTIG, O;HOCHBERG, A
基因组印记是遗传性状的单亲依赖传递，近年来已被公认为哺乳动物遗传学的主要机制。我们研究了H19基因的表达，父母印迹（母亲表达）基因，在人类胎盘和滋养细胞疾病的原位杂交。在中间滋养层（绒毛和间质）、细胞滋养层和合胞体滋养层中，发现表达丰富，以降序排列。绒毛间质也被显著标记。部分性葡萄胎的表达模式与正常胎盘相似。正如所料，完全性葡萄胎，其基因组由两套父系来源的单倍体组成，在绒毛间质和周围滋养层中没有标记。然而，一些大的单核细胞在增殖组从绒毛表面发芽强烈标记。H19在胎盘部位滋养细胞肿瘤和妊娠绒毛膜癌中表达显著。根据其起源配子而受到抑制的等位基因的表达出现的现象被称为印记松弛，并且被认为与肿瘤发生有关。我们认为，母源性表达的H19基因在雄激素组织的完全性葡萄胎代表放松的印记，并可能与其恶性潜力。(C)1994年出版社出版。
Genomic imprinting-the uniparental-dependent transmittance of a genetic trait-has been accepted in recent years as a major mechanism in mammalian genetics. We studied the expression of the H19 gene, a parentally imprinted (maternally expressed) gene, by in situ hybridization in human placenta and trophoblastic disease. Expression was found to be abundant, in a decreasing order, in the intermediate trophoblast (villous and interstitial), the cytotrophoblast, and the syncytiotrophoblast. The villous stroma was also prominently labeled. Partial hydatidiform mole showed a similar pattern of expression as normal placenta. As expected, complete hydatidiform mole, whose genome consists of two haploid sets of paternal origin, was not labeled in the villous stroma and surrounding trophoblastic layer. However, some of the large mononuclear cells in the proliferating groups sprouting from the villous surface were strongly labeled. Prominent expression of H19 was found in placental site trophoblastic tumor and gestational choriocarcinoma. The phenomenon of emergence of expression of alleles subject to repression according to their gamete of origin is termed relaxation of imprinting, and is considered to be relevant to tumorigenesis. We suggest that the expression of the maternally expressed H19 gene in the androgenetic tissue of complete hydatidiform mole represents relaxation of imprinting and may be associated with its malignant potential. (C) 1994 Academic Press, Inc.