TISSUE INTERACTIONS AND PROSTATIC GROWTH .1. INDUCTION OF ADULT-MOUSE PROSTATIC HYPERPLASIA BY FETAL UROGENITAL SINUS IMPLANTS

TISSUE INTERACTIONS AND PROSTATIC GROWTH .1. INDUCTION OF ADULT-MOUSE PROSTATIC HYPERPLASIA BY FETAL UROGENITAL SINUS IMPLANTS
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DOI:
10.1095/biolreprod31.1.155
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发表时间:
1984-01-01
影响因子:
3.6
通讯作者:
RUNNER, MN
RUNNER, MN
中科院分区:
生物学2区
文献类型:
--
作者:
CHUNG, LWK;MATSUURA, J;RUNNER, MN

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将完整的胎儿尿生殖窦(ES)植入成年裸鼠的腹侧前列腺体(VP)内,制成同种嵌合前列腺。植入UGS后4~9wk,以腺体湿重和DNA含量衡量,前列腺腹侧嵌合叶的过度生长约为对照组的10~20倍。组织学组成和对内源性雄激素的反应表明,细胞过度生长呈前列腺样,葡萄糖磷酸异构酶同工酶显示,宿主细胞和供体细胞的比例大致相同。与犬前列腺增生模型不同,小鼠前列腺过度生长是在完全没有外源性类固醇的情况下发生的。嵌合VP的组织结构和宿主细胞对过度生长的贡献的同工酶检测提供了强有力的证据,表明成年前列腺细胞通过与胎儿UGS的细胞相互作用而被招募来进行增殖反应。细胞间的相互作用以及胎儿生长潜能的重新激活为麦克尼尔的S假说提供了直接的实验证据,该假说认为胎儿生长潜能的重新激活可能是人类良性前列腺增生症(BPH)发生的原因。
A homologous chimeric prostate was produced by implantation of intact fetal urogenital sinus(es) (UGS) into the ventral prostate gland (VP) of an adult athymic mouse. A 10- to 20-fold overgrowth of the chimeric lobe of ventral prostate gland, as measured by glandular wet weight and by DNA content, was observed 4-9 wk following UGS implantation. The overgrowth was prostate-like as indicated by histologic composition and by responses to endogenous androgen, and was composed of both host and donor cells in about equal proportions as shown by glucose phosphate isomerase isozymic profiles. Unlike the canine model for prostatic hyperplasia, the mouse prostatic overgrowth occurred in the complete absence of exogenous sex steroids. The histoarchitecture of the chimeric VP and the isozymic detection of the contribution to the overgrowth by host cells have provided strong evidence that adult prostatic cells have been recruited to respond proliferatively by cellular interactions with fetal UGS. The demonstration of cellular interactions followed by reactivation of the fetal growth potential provides direct experimental evidence in support of McNeal''s hypothesis that the reactivation of fetal growth potential may account for the development of human benign prostatic hyperplasia (BPH).