Saito M, Wada Y, Ikeda K, Wang Z, Foster H E, Smith S D, Weiss R M, Latifpour J
Section of Urology, Yale University School of Medicine, New Haven, Connecticut 06520, USA.
Mol Cell Biochem. 2000 Jul;210(1-2):1-12. doi: 10.1023/a:1007041909477.
Streptozotocin (STZ)-induced diabetes causes an upregulation in the expression of endothelin (ET) receptors in the rat prostate (Eur J Pharmacol 310:197, 1996). We examined the effects of insulin treatment, started 8 weeks after the induction of diabetes, on the expression and distribution of ET receptors and their respective mRNAs in the rat prostate. The densities, pharmacological properties and distribution of ET receptors in the rat prostate were examined using radioligand receptor binding and autoradiographic studies, and gene expression of ET receptors was evaluated utilizing the reverse transcription-polymerase chain reaction (RT-PCR). STZ-injected rats had smaller prostates and reduced serum testosterone levels than control and insulin treated diabetic animals. ET receptor density was shown to be significantly higher in the prostate from diabetic rats than those from either control or insulin treated diabetic animals. The pharmacological profile of prostatic ET receptors was similar in all groups (approximately 80% ET(A); 20% ET(B) subtype). ET receptors were predominantly localized to the prostatic stroma. Induction of diabetes increased the expression of mRNA levels of ET(A) and ET receptors, and insulin treatment reversed this upregulation to control levels. These results indicate that (1) ET receptor subtypes are expressed in the rat prostate as transcription and translation products; (2) insulin can normalize the diabetes-induced upregulation in the expression of ET receptors and their respective mRNAs; and (3) diabetes-induced regression of the prostate may involve an alteration in ET receptors.
链脲佐菌素(STZ)诱导的糖尿病导致大鼠前列腺中内皮素(ET)受体的表达上调(《欧洲药理学杂志》310:197,1996)。我们研究了在糖尿病诱导8周后开始的胰岛素治疗对大鼠前列腺中ET受体及其各自mRNA的表达和分布的影响。使用放射性配体受体结合和放射自显影研究检查大鼠前列腺中ET受体的密度、药理学特性和分布,并利用逆转录-聚合酶链反应(RT-PCR)评估ET受体的基因表达。与对照和胰岛素治疗的糖尿病动物相比,注射STZ的大鼠前列腺较小且血清睾酮水平降低。结果显示,糖尿病大鼠前列腺中的ET受体密度显著高于对照或胰岛素治疗的糖尿病动物。所有组中前列腺ET受体的药理学特征相似(约80%为ET(A);20%为ET(B)亚型)。ET受体主要定位于前列腺基质。糖尿病的诱导增加了ET(A)和ET受体mRNA水平的表达,而胰岛素治疗将这种上调逆转至对照水平。这些结果表明:(1)ET受体亚型在大鼠前列腺中作为转录和翻译产物表达;(2)胰岛素可使糖尿病诱导的ET受体及其各自mRNA表达上调恢复正常;(3)糖尿病诱导的前列腺萎缩可能涉及ET受体的改变。