Normal prostate morphology in relaxin-mutant mice.

Normal prostate morphology in relaxin-mutant mice.
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松弛素突变小鼠的正常前列腺形态。

DOI:
10.1071/rd08133
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发表时间:
2009
期刊:
Reproduction, fertility, and development
影响因子:
--
通讯作者:
Parry,LauraJ
Parry,LauraJ
中科院分区:
--
文献类型:
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作者:
Ganesan,Avinash;Klonisch,Thomas;McGuane,JonathanT;Feng,Shu;Agoulnik,AlexanderI;Parry,LauraJ

文献摘要

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肽激素松弛素在前列腺中表达并分泌到精浆中;然而,其在前列腺中的功能尚未确定。松弛素突变型小鼠(Rln-/-)前列腺形态异常,而松弛素受体突变型小鼠(Rxfp 1-/-)无前列腺表型。本研究旨在验证Rln-/-和Rxfp 1-/-小鼠前列腺前叶、背叶和侧叶在不同成年年龄的表型。还用松弛素处理Rln-/-小鼠以评估外源性施用的激素对前列腺形态的影响。这三个前列腺叶之间的比较表明,在2、4、6、8和12月龄的Rln+/+和Rln-/-小鼠之间,导管形态、上皮高度或胶原蛋白密度没有明显差异。这在Rxfp 1-/-小鼠中是相似的。松弛素治疗不影响形态或上皮细胞的高度在不同的叶。此外,在过表达松弛素Tg(Rln)的转基因小鼠的前列腺叶形态与野生型对照没有不同。rxfp 1在整个成年人的前列腺中检测到,但松弛素没有一致的表达。总之,本研究没有发现支持成年Rln或Rxfp 1突变小鼠前列腺表型的证据。
The peptide hormone relaxin is expressed in the prostate gland and secreted into the seminal plasma; however, its function within the prostate has not been established. Relaxin-mutant mice (Rln–/–) were reported to have abnormal prostate morphology, but there was no prostate phenotype in relaxin receptor-mutant (Rxfp1–/–) mice. The present study aimed to verify the phenotypes in the anterior, dorsal and lateral lobes of the prostate gland of Rln–/– and Rxfp1–/– mice at different adult ages. Rln–/– mice were also treated with relaxin to evaluate the effects of exogenously administered hormone on prostate morphology. Comparisons between these three lobes of the prostate demonstrated no obvious differences in duct morphology, epithelial height or collagen density between Rln+/+ and Rln–/– mice at 2, 4, 6, 8 and 12 months of age. This was similar in Rxfp1–/– mice. Relaxin treatment did not affect morphology or epithelial cell height in the different lobes. Furthermore, prostate lobe morphology in transgenic mice overexpressing relaxin Tg(Rln) was not different from the wild-type controls. Rxfp1 was detected in the prostate throughout adult life, but there was no consistent expression of relaxin. In summary, the present study found no evidence to support a prostate phenotype in adult Rln- or Rxfp1-mutant mice.