Mandel Center for Hypertension and Atherosclerosis Research and the Cardiovascular Research Center, Duke University Medical Center, Durham, NC 27710, USA.
J Am Soc Nephrol. 2013 Jul;24(8):1263-73. doi: 10.1681/ASN.2012060596. Epub 2013 Jun 6.
The renin-angiotensin-aldosterone system (RAAS) regulates BP and salt-volume homeostasis. Juxtaglomerular (JG) cells synthesize and release renin, which is the first and rate-limiting step in the RAAS. Intense pathologic stresses cause a dramatic increase in the number of renin-producing cells in the kidney, termed JG cell recruitment, but how this occurs is not fully understood. Here, we isolated renal CD44(+) mesenchymal stem cell (MSC)-like cells and found that they differentiated into JG-like renin-expressing cells both in vitro and in vivo. Sodium depletion and captopril led to activation and differentiation of these cells into renin-expressing cells in the adult kidney. In summary, CD44(+) MSC-like cells exist in the adult kidney and can differentiate into JG-like renin-producing cells under conditions that promote JG cell recruitment.
肾素-血管紧张素-醛固酮系统(RAAS)调节血压和盐-体积稳态。肾小球旁器(JG)细胞合成并释放肾素,这是 RAAS 的第一步也是限速步骤。强烈的病理应激导致肾脏中产生肾素的细胞数量急剧增加,称为 JG 细胞募集,但这是如何发生的尚不完全清楚。在这里,我们分离了肾脏 CD44(+)间充质干细胞(MSC)样细胞,并发现它们在体外和体内都分化为具有 JG 样表达肾素的细胞。钠耗竭和卡托普利导致这些细胞在成年肾脏中激活和分化为表达肾素的细胞。总之,CD44(+)MSC 样细胞存在于成年肾脏中,并且可以在促进 JG 细胞募集的条件下分化为 JG 样肾素产生细胞。