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Developmental expression of two CXC chemokines, MIP-2 and KC, and their receptors.

机译:两种CXC趋化因子MIP-2和KC及其受体的发育表达。

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CXC chemokines, macrophage inflammatory protein-2 (MIP-2) and KC, (a cloning designation based on ordinate and abscissa position) as well as the CXC chemokine receptor, CXCR2, are expressed in a variety of cells and tissues in adult mice. Targeted deletion of the gene encoding murine CXCR2 does not result in obvious changes in the development of the organ system of the mouse, though the CXCR2-/- mouse is compromised with regard to its ability to resist infection, heal wounds, and maintain homeostasis when challenged with microbes and/or chemicals. In an attempt to develop insight into additional possible subtle roles of CXCR2 and its ligands in the development of the mouse, we examined the expression of MIP-2, KC, CXCR2, as well as the Duffy antigen binding protein for chemokines during embryonic (p.c.) days 11.5 through 14.5 in the mouse. We observed strong correlation between the expression of MIP-2 and CXCR2 in the developing brain, cardiovascular system and condensing mesenchyme between 11.5 and 13.5 days. Moreover, the expression of KC was parallel to the expression of the Duffy antigen binding protein for chemokines with regard to temporal pattern and tissue localization. MIP-2 and CXCR2 are highly expressed in the brain, first in the cerebellum and in the head mesenchyme, the meninges and the floor plate, and by 14.5 days are also present in the telencephalon, thalamus and hypothalamus. In the developing brain KC and Duffy were prominently expressed in the neuronal tracts, the forebrain, sympathetic ganglia, and along the periphery of the neural tube. However, KC and Duffy were less prevalent in the developing cardiovascular system, lung and other organs, muscle and bone, than are CXCR2 and MIP-2. These data suggest that the roles for these chemokines and their receptors during development may be more significant than was initially thought based upon the phenotype of the mice with targeted deletion of CXCR2 and Duffy. Copyright 2001 Academic Press.
机译:CXC趋化因子,巨噬细胞炎症蛋白2(MIP-2)和KC(基于纵坐标和横坐标的克隆名称)以及CXC趋化因子受体CXCR2在成年小鼠的各种细胞和组织中表达。尽管CXCR2-/-小鼠在抵抗感染,治愈伤口和维持体内平衡的能力方面受到损害,但靶向缺失小鼠CXCR2编码基因并不会导致小鼠器官系统的发育发生明显变化。受到微生物和/或化学物质的挑战。为了试图深入了解CXCR2及其配体在小鼠发育中的其他可能的微妙作用,我们检查了MIP-2,KC,CXCR2以及达菲(Duffy)抗原结合蛋白在胚胎期(pc)的表达。 )从11.5天到14.5天。我们观察到MIP-2和CXCR2在发育中的大脑,心血管系统与凝集的间充质之间的强烈相关性在11.5至13.5天之间。而且,就时间模式和组织定位而言,KC的表达与趋化因子的达菲抗原结合蛋白的表达平行。 MIP-2和CXCR2在大脑中高度表达,首先在小脑和头部间质,脑膜和底板中表达,到14.5天时,在远脑,丘脑和下丘脑中也存在。在发育中的大脑中,KC和Duffy在神经元束,前脑,交感神经节以及沿神经管的外围突出表达。然而,与CXCR2和MIP-2相比,KC和Duffy在发展中的心血管系统,肺和其他器官,肌肉和骨骼中的流行率较低。这些数据表明,这些趋化因子及其受体在发育过程中的作用可能比基于基于CXCR2和Duffy靶向缺失的小鼠表型的最初设想更为重要。版权所有2001,学术出版社。

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