TY - JOUR
T1 - Analysis of Kif5b expression during mouse kidney development
AU - Cui, Ju
AU - Li, Xiuling
AU - Duan, Zhigang
AU - Xue, Wenqian
AU - Wang, Zai
AU - Lu, Song
AU - Lin, Raozhou
AU - Liu, Mengfei
AU - Zhu, Guixia
AU - Huang, Jian Dong
N1 - Publisher Copyright:
© 2015 Cui et al.
PY - 2015/4/17
Y1 - 2015/4/17
N2 - 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 themouse 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 inmouse kidney. Kidneys fromembryonic (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 bornmice, 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 capmesenchyme, 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 detectablemorphological defects, but it did lead to a decrease in cell proliferation rate and also to amislocalization of Na+/K+/-ATPase, indicating that although Kif5b is non-essential for kidneymorphogenesis, it is important for nephron maturation.
AB - 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 themouse 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 inmouse kidney. Kidneys fromembryonic (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 bornmice, 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 capmesenchyme, 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 detectablemorphological defects, but it did lead to a decrease in cell proliferation rate and also to amislocalization of Na+/K+/-ATPase, indicating that although Kif5b is non-essential for kidneymorphogenesis, it is important for nephron maturation.
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U2 - 10.1371/journal.pone.0126002
DO - 10.1371/journal.pone.0126002
M3 - Article
C2 - 25885434
AN - SCOPUS:84929494350
SN - 1932-6203
VL - 10
JO - PLoS One
JF - PLoS One
IS - 4
M1 - e0126002
ER -