MICE DEFICIENT FOR PDGF-B SHOW RENAL, CARDIOVASCULAR, AND HEMATOLOGICAL ABNORMALITIES
MICE DEFICIENT FOR PDGF-B SHOW RENAL, CARDIOVASCULAR, AND HEMATOLOGICAL ABNORMALITIES
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DOI：
10.1101/gad.8.16.1875
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发表时间：
1994-08-15
影响因子：
10.5
通讯作者：
BETSHOLTZ, C
中科院分区：
文献类型：
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作者：
LEVEEN, P;PEKNY, M;BETSHOLTZ, C
血小板源性生长因子（PDGE）在体外影响间充质细胞的生长、迁移和功能，但其在体内的正常生理功能却知之甚少。我们在这里表明，缺乏PDGF B的小鼠围产期死亡，并显示一些解剖和组织学异常。肾小球簇不形成，显然是因为缺乏系膜细胞。相反，一个或几个扩张的毛细血管袢填充肾小球空间。心脏和一些大动脉在胚胎后期扩张。大多数PDGF B突变胚胎在出生前发生致命性发育不良。他们的血液学状态包括成红细胞增多症、巨红细胞性贫血和血小板减少症。基于这些发现，我们得出结论，PDGE B在体内建立某些肾脏和循环功能中具有关键作用。
Platelet-derived growth factor (PDGE) affects the growth, migration, and function in vitro of mesenchymal cells, but little is known about its normal physiological functions in vivo. We show here that mice deficient for PDGF B die perinatally and display several anatomical and histological abnormalities. Kidney glomerular tufts do not form, apparently because of absence of mesangial cells. Instead, a single or a few distended capillary loops fill the glomerular space. The heart and some large arteries dilate in late-stage embryos. Most PDGF B mutant embryos develop fatal hemorrhages just prior to birth. Their hematological status includes erythroblastosis, macrocytic anemia, and thrombocytopenia. On the basis of these findings, we conclude that PDGE B has crucial roles in vivo in establishing certain renal and circulatory functions.