Yang C W, Striker L J, Kopchick J J, Chen W Y, Pesce C M, Peten E P, Striker G E
Renal Cell Biology Section, National Institute of Diabetes, Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland.
Kidney Int Suppl. 1993 Jan;39:S90-4.
Mice transgenic for bovine growth hormone (bGH) develop an increase in body weight and glomerular lesions characterized by a disproportionate increment in glomerular volume and progressive mesangial sclerosis. The relationship between glomerular size and body growth in bGH mice was further investigated by examining mice transgenic for a mutated GH gene (bGH-m11) which failed to enhance body growth. The glomeruli in bGH-m11 mice exhibited an increase in size and glomerulosclerosis comparable to those found in bGH mice. The levels of alpha 1 type IV collagen mRNA, as measured by the competitive polymerase chain reaction in isolated microdissected glomeruli, were markedly elevated in mice transgenic for both bGH and bGH-m11 genes. These data suggest that body growth on one hand, and glomerular hypertrophy and sclerosis on the other hand, are mediated by different portions of GH or different second messenger signaling systems.
转牛生长激素(bGH)基因的小鼠体重增加,并出现肾小球病变,其特征为肾小球体积不成比例增加和进行性系膜硬化。通过检查转突变生长激素基因(bGH-m11)的小鼠(该基因无法促进身体生长),进一步研究了bGH小鼠中肾小球大小与身体生长之间的关系。bGH-m11小鼠的肾小球表现出大小增加和肾小球硬化,与bGH小鼠中的情况相当。通过竞争性聚合酶链反应在分离的显微切割肾小球中测量,α1 IV型胶原mRNA水平在转bGH和bGH-m11基因的小鼠中均显著升高。这些数据表明,一方面身体生长,另一方面肾小球肥大和硬化,是由生长激素的不同部分或不同的第二信使信号系统介导的。