VEGFR-3通过PI3K/AKT信号通路促进触液神经元增殖的作用机制

Abstract
Figure/Table
References (28)
Related Citation (15)

Download: PDF (866 KB) HTML (1 KB)
Export: BibTeX | EndNote (RIS)

Abstract Objective To investigate the effect of vascular endothelial growth factor receptor-3 (VEGFR-3) on the proliferation of cerebrospinal fluid-contacting neurons (CSF-CNs) through PI3K/AKT signaling pathway. Methods CSF-CNs were isolated from ten 3-day-old C57 newborn mice, and divided into four groups: normal control group, empty plasmid control group, VEGFR-3 plasmid group and inhibitor group. The normal control group was without special treatment, empty plasmid control group added empty plasmid, and VEGFR-3 plasmid dilution was added into VEGFR-3 plasmid group, PI3K/AKT inhibitor was added into transfected cells in inhibitor group. The number and diameter of neurospheres were detected after 24 h, and the expression of VEGFR-3, PI3K, AKT, and p-AKT were detected by Western blot. Results The expression of VEGFR-3 in VEGFR-3 plasmid group was higher than that in normal control group and empty plasmid control group (P ＜ 0.05), and the transfection efficiency was the highest after 48 h. Compared with empty plasmid group and inhibitor group, the number and diameter of neurospheres in VEGFR-3 plasmid group increased (P ＜ 0.05), and the expression of PI3K, AKT, and p-AKT in VEGFR-3 plasmid group were higher (P ＜ 0.05). Conclusion VEGFR-3 can promote the proliferation of CSF-CNs by regulating PI3K/AKT signaling pathway.

Key words： Vascular endothelial growth factor receptor-3 PI3K/AKT signaling pathway Cerebrospinal fluid-contacting neurons Proliferation

	Service

	E-mail this article
	Add to my bookshelf
	Add to citation manager
	E-mail Alert
	RSS
	Articles by authors
	HU Qian YAN Haijian▲

Cite this article:

HU Qian YAN Haijian▲. Mechanism of VEGFR-3 promoting proliferation of cerebrospinal fluid-contacting neurons through PI3K/AKT signaling pathway#br#[J]. 中国医药导报, 2021, 18(34): 23-25,34.

URL:

https://www.yiyaodaobao.com.cn/EN/ OR https://www.yiyaodaobao.com.cn/EN/Y2021/V18/I34/23

[1] Zhu S，Yang BS，Li SJ，et al. Protein post-translational modifications after spinal cord injury [J]. Neural Regen Res，2021，16（10）：1935-1943.
[2] 闵令霞，刘宏亮，段霞，等.急性脊髓损伤生物标志物的研究进展[J].中国康复，2021，36（1）：45-49.
[3] 吴昌平.分析早期康复对脊髓损伤患者肢体功能及各种并发症发生率的影响[J].按摩与康复医学，2021，12（12）：48-49，52.
[4] 王栋，谢斌华，张慧芊，等.脊髓损伤大鼠触液神经元中p75NTR的表达[J].中国脊柱脊髓杂志，2017，27（4）：361-367.
[5] Orts-Del’Immagine A，Cantaut-Belarif Y，Thouvenin O，et al. Sensory Neurons Contacting the Cerebrospinal Fluid Require the Reissner Fiber to Detect Spinal Curvature In Vivo [J]. Curr Biol，2020，30（5）：827-839.e4.
[6] 李瑞，刘海鹰，王家瑶，等.触脑脊液神经元的研究进展[J].神经解剖学杂志，2018，34（5）：633-637.
[7] Maisel K，Hrusch CL，Medellin JEG，et al. Pro-lymphangiogenic VEGFR-3 signaling modulates memory T cell responses in allergic airway inflammation [J]. Mucosal Immunol，2021，14（1）：144-151.
[8] 李璟波，夏晖，刘阳.肺癌中VEGF-C、VEGFR3表达与预后的关系及意义[J].中国医药导报，2020，17（6）：30-32，52.
[9] Kang TH，Han J，Thomas JL. Cell autonomous Vegf-C/Vegfr3 signaling in adult neural stem cells [J]. Oncotarget，2015，6（37）：39387-8.
[10] Djenoune L，Khabou H，Joubert F，et al. Investigation of spinal cerebrospinal fluid-contacting neurons expressing PKD2L1：evidence for a conserved system from fish to primates [J]. Front Neuroanat，2014，8（6）：000026.
[11] Beierle EA，Ma X，Stewart JE，et al. Inhibition of the focal adhesion kinase and vascular endothelial growth factor receptor-3 interaction leads to decreased survival in human neuroblastoma cell lines [J]. Mol Carcinog，2014， 53（3）：230-242.
[12] Alibardi L. Cerebrospinal fluid-contacting neurons in the regenerating spinal cord of lizards and amphibians are likely mechanoreceptors [J]. J Morphol，2019，280（9）：1292-1308.
[13] 涂源源，刘亦恒，邢晓伟.苯甲酸钠通过抑制线粒体凋亡保护大鼠脊髓损伤的研究[J].中国临床药理学杂志，2021，37（11）：1394-1399.
[14] 梅运运，张建军，王东.高压氧联合NgR基因沉默骨髓间充质干细胞移植治疗大鼠脊髓损伤[J].中国组织工程研究，2022，26（1）：12-19.
[15] Kong FL，Wang XP，Li YN，et al. The role of exosomes derived from cerebrospinal fluid of spinal cord injury in neuron proliferation in vitro [J]. Artif Cells Nanomed Biotechnol，2018，46（1）：200-205.
[16] 韩旭，余清文，刘京津，等.心理支持护理对脊髓损伤患者心理康复的影响[J].现代消化及介入诊疗，2019（A01）：2.
[17] 吴番娜，向阳，牛英杰，等.白细胞介素-10对大鼠脊髓钝挫伤修复的影响及机制研究[J].成都医学院学报，2020，15（2）：7.
[18] 何宇祺.Notch1信号通路调节触液神经元增殖能力的研究[D].贵阳：贵州医科大学，2020.
[19] 何宇祺，林宗龙，王硕，等.Notch1信号通路对小鼠触液神经元体外增殖能力的调节作用[J].中国脊柱脊髓杂志，2021，31（3）：262-270.
[20] 谢斌华.脊髓损伤大鼠中触液神经元ERK5的表达情况分析[D].贵阳：贵州医科大学，2017.
[21] 王玉玲，暴亚锋，刘静，等.VEGFR-3在抗肿瘤淋巴管生成中研究进展[J].生命的化学，2017，37（5）：772-776.
[22] Wu H，Rahman HNA，Dong Y，et al. Epsin deficiency promotes lymphangiogenesis through regulation of VEGFR3 degradation in diabetes [J]. J Clin Invest，2018，128（9）：4025-4043.
[23] Kumar R，Mani AM，Singh NK，et al. PKCθ-JunB axis via upregulation of VEGFR3 expression mediates hypoxia-induced pathological retinal neovascularization [J]. Cell Death Dis，2020，11（5）：325.
[24] 杨婷婷，李鹏运，郑志兵.VEGFR小分子抑制剂研究的新进展[J].军事医学，2021，45（5）：390-396.
[25] Tacconi C，Ungaro F，Correale C，et al. Activation of the VEGFC/VEGFR3 Pathway Induces Tumor Immune Escape in Colorectal Cancer [J]. Cancer Res，2019，79（16）：4196-4210.
[26] 聂晶鑫，尚静波，孟庆涛.槲皮素对脊髓损伤大鼠神经元自噬及PI3K/Akt通路的影响[J].中国中医急症，2020， 29（8）：1415-1419，1439.
[27] Jiang N，Dai Q，Su X，et al. Role of PI3K/AKT pathway in cancer：the framework of malignant behavior [J]. Mol Biol Rep，2020，47（6）：4587-4629.
[28] 陈鹤，王永乐.基于PI3K-Akt-eNOS通路探讨松果菊苷对脊髓损伤大鼠的神经保护作用[J].中国中医急症，2019，28（10）：1721-1725，1729.