Knocking down B7H3 expression enhances cell proliferation of SHEDs via the SHR1/AKT signal axis
Knocking down B7H3 expression enhances cell proliferation of SHEDs via the SHR1/AKT signal axis
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敲低 B7H3 表达可通过 SHR1/AKT 信号轴增强 SHED 的细胞增殖
DOI：
10.1016/j.bbrc.2020.06.154
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发表时间：
2020-10-20
影响因子：
3.1
通讯作者：
Zhu, Dongwang
中科院分区：
文献类型：
--
作者：
Chen, Gang;Tu, Yaoyao;Zhu, Dongwang
B7 H3是免疫调节跨膜糖蛋白B7家族的成员，与维持免疫耐受、肿瘤细胞增殖、迁移、侵袭和代谢、耐药性以及干细胞分化相关。牙髓神经嵴来源的多能干细胞（MSCs）因其来源简单、再生能力强而成为组织再生的良好选择。虽然已经有许多研究调查B7 H3在癌细胞和免疫细胞中的作用，但其在牙髓干细胞再生中的作用尚不清楚。本研究选择人脱落乳牙干细胞（SHEDs）作为研究模型，分析B7 H3的表达和功能。结果表明，SHEDs呈B7 H3/CD 90、B7 H3/CD 73、B7 H3/CD 105双阳性，B7 H3主要表达于细胞膜。下调B7 H3表达通过SHP 1/AKT信号轴显著加速SHED的扩增，而上调B7 H3表达降低SHED的增殖。因此，本研究表明，B7 H3是干细胞表面分子，并可能被用作SHED标记物，由此其下调通过激活B7 H3/SHP 1/AKT信号通路增强SHED的增殖。(C)2020爱思唯尔公司All rights reserved.
B7H3 is a member of B7 family of immunoregulatory transmembrane glycoproteins associated with maintaining immune tolerance, tumor cell proliferation, migration, invasion and metabolism, drug resistance, and stem cell differentiation. Neural crest-derived Multipotent Stem Cells (MSCs) from the dental pulp has become a good choice for tissue regeneration because it is easily obtainable and has strong regeneration potentials. Although there have been many studies investigating the role of B7H3 in cancer cells and immune cells, its role in the dental pulp stem cells regeneration is unknown. In this study, we chose SHEDs (stem cells from human exfoliated deciduous teeth) as a research model to analyze the expression and function of B7H3. The result showed that SHEDs were B7H3/CD90, B7H3/ CD73, B7H3/CD105 double positive, and the expression of B7H3 is primarily located within the membrane. Downregulation of B7H3 expression significantly accelerated the expansion of SHEDs through the SHP1/AKT signal axis while upregulation of B7H3 expression decreased the proliferation of SHEDs. Hence, this study indicates that B7H3 is a stem cell surface molecule and might be used as a SHEDs marker whereby its downregulation enhances the proliferation of SHEDs via the activation of B7H3/ SHP1/AKT signaling pathway. (C) 2020 Elsevier Inc. All rights reserved.