Wang C, Chen Y P, Chao L, Chao J
Department of Biochemistry and Molecular Biology, Medical University of South Carolina, Charleston 29425, USA.
Biochem Biophys Res Commun. 1995 Dec 5;217(1):113-22. doi: 10.1006/bbrc.1995.2752.
The renal kallikrein-kinin system has been implicated in the pathogenesis of hypertension. The expression level of the renal kallikrein gene in the kidney is significantly lower in spontaneously hypertensive rats (SHR) as compared with that of normotensive (SD and WKY) rats. Deletion analysis showed that the fragment -356/-188 of the promoter contains a transcriptional silencer(s) and the GC rich region located between -77 and -187 is the minimal essential element for directing the expression of the CAT reporter gene in mouse L cells. In the kidney of normotensive vs hypertensive rats, the nuclear protein factors NF1/CTF and SP1 bind differently to the renal kallikrein promoter, but similarly in the salivary gland. The differential transcriptional regulation of the rat renal kallikrein gene in the kidney may be responsible for the genetic difference between normotensive and hypertensive rats.
肾激肽释放酶 - 激肽系统与高血压的发病机制有关。与正常血压（SD和WKY）大鼠相比，自发性高血压大鼠（SHR）肾脏中肾激肽释放酶基因的表达水平显著降低。缺失分析表明，启动子的-356 / -188片段含有转录沉默子，位于-77和-187之间的富含GC的区域是指导CAT报告基因在小鼠L细胞中表达的最小必需元件。在正常血压大鼠与高血压大鼠的肾脏中，核蛋白因子NF1 / CTF和SP1与肾激肽释放酶启动子的结合方式不同，但在唾液腺中相似。大鼠肾激肽释放酶基因在肾脏中的差异转录调控可能是正常血压大鼠和高血压大鼠之间遗传差异的原因。
