Johnston J M, Wood D F, Bolaji E A, Johnston D G
Unit of Metabolic Medicine, St Mary's Hospital Medical School, Imperial College of Science, Technology and Medicine, Paddington, London.
J Mol Endocrinol. 1991 Oct;7(2):131-6. doi: 10.1677/jme.0.0070131.
Some pituitary tumours respond to dopamine by decreasing the release of prolactin and/or GH and by inhibition of tumour growth. Certain tumours are unresponsive. Dopamine D2 receptor high-affinity binding is impaired in these tumours, and the rat GH3 cell line behaves in a similar way. The hypothesis that the dopamine-binding defect results from impaired D2 receptor gene expression has been tested in the present study. On Northern blots, D2 receptor mRNA was present in both normal rat pituitary cells and in GH3 cells. Sodium dodecyl sulphate-polyacrylamide gel electrophoresis identified a putative D2 receptor protein in normal and GH3 cell membranes. The lack of effect of dopamine in GH3 cells does not reflect the absence of D2 receptor gene expression.
一些垂体瘤通过减少催乳素和(或)生长激素的释放以及抑制肿瘤生长来对多巴胺产生反应。某些肿瘤则无反应。在这些肿瘤中多巴胺D2受体的高亲和力结合受损,大鼠GH3细胞系也表现出类似情况。本研究对多巴胺结合缺陷是由D2受体基因表达受损导致这一假说进行了验证。在Northern印迹法中,D2受体mRNA在正常大鼠垂体细胞和GH3细胞中均有存在。十二烷基硫酸钠-聚丙烯酰胺凝胶电泳在正常和GH3细胞膜中鉴定出一种假定的D2受体蛋白。多巴胺对GH3细胞无作用并不反映D2受体基因表达的缺失。