Analysis of Kif5b expression during mouse kidney development.

Analysis of Kif5b expression during mouse kidney development.
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小鼠肾脏发育过程中 Kif5b 表达的分析。

DOI:
10.1371/journal.pone.0126002
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发表时间:
2015
期刊:
影响因子:
3.7
通讯作者:
Huang JD
Huang JD
中科院分区:
综合性期刊3区
文献类型:
--
作者:
Cui J;Li X;Duan Z;Xue W;Wang Z;Lu S;Lin R;Liu M;Zhu G;Huang JD

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最近的研究表明,肾脏特异性失活Kif 3a导致肾囊肿和肾衰竭,这表明驱动蛋白介导的细胞内转运对于建立和维持肾上皮细胞极性和正常肾单位功能是重要的。Kif 5 b是最保守的驱动蛋白重链之一,是人普遍存在的驱动蛋白重链(uKHC)的小鼠同源物。为了阐明Kif 5 b在肾脏发育和功能中的作用,必须建立其在器官内的表达谱。因此,在本研究中,我们研究了Kif 5 b在小鼠肾脏中的表达模式。收集胚胎(E)12.5-、16.5-dpc(交配后天数)小鼠胎儿、出生后(P)0、10、20天幼仔和成年小鼠的肾脏。通过免疫染色分析Kif 5 b的分布。通过使用Cre-LoxP策略在条件突变小鼠中研究Kif 5 b在肾脏发育中的可能参与。本研究表明,Kif 5 b的分布在出生后肾脏发育过程中表现出时空变化。在新生小鼠的肾脏中,Kif 5 b在所有发育中的小管和输尿管芽中强烈表达,但不在肾小球或其他早期发育的结构中,如帽间充质、逗号形体和S形体。然而,在出生后第20天或年龄较大的小鼠的肾脏中,Kif 5 b选择性地定位于Henle氏粗升袢上皮细胞的基底外侧域以及远曲小管,在近曲小管或集合管中观察到很少的表达。Kif 5 b在小鼠肾脏中的条件性敲低没有导致可检测的形态缺陷,但它确实导致细胞增殖率降低,并且还导致Na+/K+/-ATP酶的错误定位,这表明尽管Kif 5 b对于肾脏形态发生不是必需的,但它对于肾单位成熟是重要的。
Recent studies showed that kidney-specific inactivation of Kif3a produces kidney cysts and renal failure, suggesting that kinesin-mediated intracellular transportation is important for the establishement and maintenance of renal epithelial cell polarity and normal nephron functions. Kif5b, one of the most conserved kinesin heavy chain, is the mouse homologue of the human ubiquitous Kinesin Heavy Chain (uKHC). In order to elucidate the role of Kif5b in kidney development and function, it is essential to establish its expression profile within the organ. Therefore, in this study, we examined the expression pattern of Kif5b in mouse kidney. Kidneys from embryonic (E) 12.5-, 16.5-dpc (days post coitus) mouse fetuses, from postnatal (P) day 0, 10, 20 pups and from adult mice were collected. The distribution of Kif5b was analyzed by immunostaining. The possible involvement of Kif5b in kidney development was investigated in conditional mutant mice by using a Cre-LoxP strategy. This study showed that the distribution of Kif5b displayed spatiotemporal changes during postnatal kidney development. In kidneys of new born mice, Kif5b was strongly expressed in all developing tubules and in the ureteric bud, but not in the glomerulus or in other early-developing structures, such as the cap mesenchyme, the comma-shaped body, and the S-shaped body. In kidneys of postnatal day 20 or of older mice, however, Kif5b was localized selectively in the basolateral domain of epithelial cells of the thick ascending loop of Henle, as well as of the distal convoluted tubule, with little expression being observed in the proximal tubule or in the collecting duct. Conditional knock-down of Kif5b in mouse kidney did not result in detectable morphological defects, but it did lead to a decrease in cell proliferation rate and also to a mislocalization of Na+/K+/-ATPase, indicating that although Kif5b is non-essential for kidney morphogenesis, it is important for nephron maturation.
DOI: 10.1159/000076752
发表时间: 2004-01-01
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