Rashed H M, Sun H, Patel T B
Department of Pharmacology, University of Tennessee, Memphis 38163.
Hepatology. 1993 Apr;17(4):677-84. doi: 10.1002/hep.1840170423.
To investigate whether atrial natriuretic factor regulates the growth of hepatocytes and to determine the receptor subtype involved in such modulation, we studied the effect of atrial natriuretic factor 103-126 and clearance receptor binding analogs of atrial natriuretic factor, (des-(Q116, S117, G118, L119, G120) atrial natriuretic factor 102-121 and des-(C105,121) atrial natriuretic factor 104-126) on growth of human hepatoblastoma cells. Atrial natriuretic factor 103-126 and des-(Q116, S117, G118, L119, G120) atrial natriuretic factor 102-121 inhibited thymidine incorporation into human hepatoblastoma cells cultured in the presence of bovine serum albumin and epidermal growth factor but not in cells cultured in bovine serum albumin alone. Moreover, atrial natriuretic factor 103-126, des-(Q116, S117, G118, L119, G120) atrial natriuretic factor 102-121 and des-(C105,121) atrial natriuretic factor 104-126, in a concentration-dependent manner, inhibited thymidine incorporation and cell proliferation. As monitored by the ability of des-(Q116, S117, G118, L119, G120) atrial natriuretic factor 102-121 to displace 125I-labeled atrial natriuretic factor, epidermal growth factor increased the expression of cell surface clearance receptors. Epidermal growth factor also transiently increased the cellular content of atrial natriuretic factor clearance receptor messenger RNA without altering the levels of guanylyl cyclase-linked atrial natriuretic factor receptor messenger RNA levels. Maximal increase in atrial natriuretic factor clearance receptor messenger RNA coincided with the maximal increase in des-(Q116, S117, G118, L119, G120) atrial natriuretic factor 102-121-displaceable 125I-atrial natriuretic factor binding sites.(ABSTRACT TRUNCATED AT 250 WORDS)
为研究心房利钠因子是否调节肝细胞生长，并确定参与这种调节的受体亚型，我们研究了心房利钠因子103 - 126以及心房利钠因子的清除受体结合类似物（去（Q116、S117、G118、L119、G120）心房利钠因子102 - 121和去（C105,121）心房利钠因子104 - 126）对人肝母细胞瘤细胞生长的影响。心房利钠因子103 - 126和去（Q116、S117、G118、L119、G120）心房利钠因子102 - 121抑制了在牛血清白蛋白和表皮生长因子存在下培养的人肝母细胞瘤细胞对胸苷的掺入，但在仅用牛血清白蛋白培养的细胞中则没有这种作用。此外，心房利钠因子103 - 126、去（Q116、S117、G118、L119、G120）心房利钠因子102 - 121和去（C105,121）心房利钠因子104 - 126以浓度依赖的方式抑制胸苷掺入和细胞增殖。通过去（Q116、S117、G118、L119、G120）心房利钠因子102 - 121置换125I标记的心房利钠因子的能力监测发现，表皮生长因子增加了细胞表面清除受体的表达。表皮生长因子还短暂增加了心房利钠因子清除受体信使核糖核酸的细胞含量，而未改变鸟苷酸环化酶连接的心房利钠因子受体信使核糖核酸水平。心房利钠因子清除受体信使核糖核酸的最大增加与去（Q116、S117、G118、L119、G120）心房利钠因子102 - 121可置换的125I - 心房利钠因子结合位点的最大增加同时出现。（摘要截短于250字）
