ELEVATED C-MYC PROTOONCOGENE EXPRESSION IN AUTOSOMAL RECESSIVE POLYCYSTIC KIDNEY-DISEASE
ELEVATED C-MYC PROTOONCOGENE EXPRESSION IN AUTOSOMAL RECESSIVE POLYCYSTIC KIDNEY-DISEASE
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DOI：
10.1073/pnas.84.23.8394
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发表时间：
1987-12-01
影响因子：
11.1
通讯作者：
CALVET, JP
中科院分区：
文献类型：
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作者：
COWLEY, BD;SMARDO, FL;CALVET, JP
多囊肾病（pkd）是一组以肾单位和肾小管集合管上皮囊肿生长为特征的疾病。这些疾病可以遗传，也可以由环境因素引起。为了研究与PKD相关的异常细胞生长的分子基础，我们在常染色体隐性PKD小鼠模型中研究了c-myc原癌基因的表达。纯合隐性C57BL/6J （cpk/cpk）小鼠在3周龄后出现大量增大的囊性肾脏并死于肾功能衰竭。将全肾poly(A)+ RNA与c-myc RNA探针杂交的定量斑点杂交和RNA杂交实验显示，与正常窝鼠相比，多囊小鼠在2周龄时c-myc mRNA增加了2- 6倍，在3周龄时c-myc mRNA增加了25- 30倍。C-myc的表达也在两种条件下进行了检测，这两种条件是正常成年小鼠实验性诱导肾细胞生长：代偿性肾肥大和叶酸诱导肾细胞损伤后的小管再生。代偿性肥厚只导致一小部分(
The polycystic kidney diseases (PKDs) are a group of disorders characterized by the growth of epithelial cysts from the nephrons and collecting ducts of kidney tubules. The diseases can be inherited or can be provoked by environmental factors. To investigate the molecular basis of the abnormal cell growth associated with PKD, c-myc protooncogene expression was studied in a mouse model for autosomal recessive PKD. Homozygous recessive C57BL/6J (cpk/cpk) mice develop massively enlarged cystic kidneys and die from renal failure shortly after 3 weeks of age. Quantitative dot blot and RNA blot hybridization experiments in which whole kidney poly(A)+ RNA was hybridized with a c-myc RNA probe showed a 2- to 6-fold increase in c-myc mRNA at 2 weeks, and a 25- to 30-fold increase in c-myc mRNA at 3 weeks of age in polycystic mice, as compared to normal littermates. c-myc expression was also examined under two conditions in which kidney cell growth was experimentally induced in normal adult mice: compensatory renal hypertrophy and tubule regeneration following folic acid-induced renal cell injury. While compensatory hypertrophy resulted in only a small (