Suppr超能文献

组织相互作用与前列腺生长。I. 胎儿泌尿生殖窦植入物诱导成年小鼠前列腺增生

Tissue interactions and prostatic growth. I. Induction of adult mouse prostatic hyperplasia by fetal urogenital sinus implants.

作者信息

Chung L W, Matsuura J, Runner M N

出版信息

Biol Reprod. 1984 Aug;31(1):155-63. doi: 10.1095/biolreprod31.1.155.

Abstract

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 to 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).

摘要

通过将完整的胎儿泌尿生殖窦(UGS)植入成年无胸腺小鼠的腹侧前列腺(VP),构建了一个同源嵌合前列腺。UGS植入后4至9周,通过腺体湿重和DNA含量测量发现,腹侧前列腺的嵌合叶出现了10至20倍的过度生长。从组织学组成和对内源性雄激素的反应来看,这种过度生长类似前列腺,并且如磷酸葡萄糖异构酶同工酶谱所示,宿主细胞和供体细胞的比例大致相等。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性激素的情况下发生的。嵌合VP的组织结构以及宿主细胞对过度生长贡献的同工酶检测提供了有力证据,表明成年前列腺细胞已被募集,通过与胎儿UGS的细胞相互作用进行增殖反应。细胞相互作用后胎儿生长潜能的重新激活的证明,为支持麦克尼尔的假设提供了直接的实验证据,即胎儿生长潜能的重新激活可能是人类良性前列腺增生(BPH)发生的原因。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验