Expression of Urea Transporter B in Normal and Injured Brain.
Expression of Urea Transporter B in Normal and Injured Brain.
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尿素转运蛋白 B 在正常和损伤脑中的表达
DOI：
10.3389/fnana.2021.591726
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发表时间：
2021
影响因子：
2.9
通讯作者：
Ran J
中科院分区：
文献类型：
--
作者：
Huang B;Wang H;Zhong D;Meng J;Li M;Yang B;Ran J
尿素转运蛋白B（UT - B）是一种广泛分布于哺乳动物体内的膜通道蛋白，通过调节不同组织中的尿素和水转运发挥重要的生理作用。越来越多的研究发现，UT - B与神经系统疾病相关，包括髓鞘病和抑郁症。当尿素在UT - B基因敲除小鼠的大脑中积累时，神经元的突触可塑性降低，神经胶质细胞的形态和功能也会发生改变。然而，UT - B的分布和表达变化仍不明确。本研究旨在确定UT - B在大脑中的表达特征。通过单细胞RNA测序发现，除内皮细胞和平滑肌细胞外，UT - B在中枢神经系统的各种细胞中普遍且大量表达。通过免疫组织化学方法，在第三脑室壁、齿状回颗粒细胞层以及海马、大脑皮层、黑质、缰核和下丘脑外侧核的其他部位检测到了UT - B。与UT - B在神经胶质细胞中的膜表达相比，UT - B在神经元中的亚细胞定位在高尔基体。此外，在体外，UT - B的表达受渗透压调节。在实验性创伤性脑损伤模型（TBI）中，同侧大脑皮层附近UT - B阳性神经元的数量随时间先增加后减少，在24小时时达到峰值。我们推断，TBI后UT - B表达的变化是对尿素水平改变的一种适应。实验数据表明，UT - B可能是治疗TBI和白质水肿的潜在靶点。
Urea transporter B (UT-B) is a membrane channel protein widely distributed in mammals, and plays a significant physiological role by regulating urea and water transportation in different tissues. More and more studies have found that UT-B is related to neurological diseases, including myelinopathy and depression. When urea accumulates in the brains of UT-B knockout mice, the synaptic plasticity of neurons is reduced, and the morphology and function of glial cells are also changed. However, the distribution and expression change of UT-B remain unclear. The purpose of this study is to determine the expression characteristics of UT-B in the brain. Through single-cell RNA sequencing, UT-B was found to express universally and substantially throughout the various cells in the central nervous system except for endothelial and smooth muscle cells. UT-B was detected in the third cerebral ventricular wall, granule cell layer of the dentate gyrus, and other parts of the hippocampal, cerebral cortex, substantia nigra, habenular, and lateral hypothalamic nucleus by immunohistochemistry. Compared with the membrane expression of UT-B in glial cells, the subcellular localization of UT-B is in the Golgi apparatus of neurons. Further, the expression of UT-B was regulated by osmotic pressure in vitro. In the experimental traumatic brain injury model (TBI), the number of UT-B positive neurons near the ipsilateral cerebral cortex increased first and then decreased over time, peaking at the 24 h. We inferred that change in UT-B expression after the TBI was an adaptation to changed urea levels. The experimental data suggest that the UT-B may be a potential target for the treatment of TBI and white matter edema.
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DOI：
10.1152/ajprenal.00359.2001
发表时间：
2002-11-01
影响因子：
4.2
作者：
Trinh-Trang-Tan, MM;Lasbennes, F;Bailly, P
通讯作者：
Bailly, P
影响因子：
5.3
作者：
DORNAY, M;GILAD, VH;GILAD, GM
通讯作者：
GILAD, GM
影响因子：
64.8
作者：
Tanay A;Regev A
通讯作者：
Regev A
DOI：
10.1007/s004290050152
发表时间：
1998-05-01
期刊：
ANATOMY AND EMBRYOLOGY
影响因子：
--
作者：
Berger, UV;Tsukaguchi, H;Hediger, MA
通讯作者：
Hediger, MA
影响因子：
--
作者：
PALLONE, TL
通讯作者：
PALLONE, TL