Ito Mayuko, Nishizawa Haruki, Tsutsumi Makiko, Kato Asuka, Sakabe Yoshiko, Noda Yoshiteru, Ohwaki Akiko, Miyazaki Jun, Kato Takema, Shiogama Kazuya, Sekiya Takao, Kurahashi Hiroki, Fujii Takuma
Department of Obstetrics and Gynecology, Fujita Health University School of Medicine, 1-98 Dengakugakubo, Kutsukake, Toyoake, Aichi, 470-1192, Japan.
Division of Molecular Genetics, Institute for Comprehensive Medical Science, Fujita Health University, Toyoake, Japan.
BMC Med Genet. 2018 Sep 14;19(1):166. doi: 10.1186/s12881-018-0681-y.
Nectins are cell adhesion molecules that play a pivotal role in adherens junctions and tight junctions. Our previous study using whole-genome oligonucleotide microarrays revealed that nectin-4 was upregulated in pre-eclamptic placentas. We investigated the role of nectin-4 in the etiology of pre-eclampsia.
We investigated the expression of nectin-4 using real-time RT-PCR, western blot and immunostaining. Additionally, we performed matrigel invasion assay and cytotoxicity assay using cells overexpressing the nectin-4.
NECTIN4 transcripts were elevated in pre-eclamptic placentas relative to uncomplicated pregnancies. Nectin-4 protein levels in pre-eclamptic placentas were higher on a semi-quantitative western blot. Nectin-4 was localized at the apical cell membrane in syncytiotrophoblast cells and not at the adherens junctions. Nectin-4 was also detected in cytotrophoblasts and a subset of cells in the decidua. Nectin-4 overexpressing trophoblast cells migrated normally in the matrix. However, Natural killer (NK) cells showed a strong cytotoxic effect against nectin-4 overexpressing trophoblast cells. No causative genetic variation was evident in the NECTIN4 gene from a pre-eclamptic placenta.
There are as yet unknown factors that induce nectin-4 overexpression in trophoblast cells that may contribute to abnormal placentation via an aberrant immune response and the onset of a pre-eclamptic pregnancy.
NECTIN蛋白是细胞黏附分子,在黏着连接和紧密连接中起关键作用。我们之前使用全基因组寡核苷酸微阵列进行的研究显示,NECTIN-4在子痫前期胎盘组织中表达上调。我们研究了NECTIN-4在子痫前期病因学中的作用。
我们使用实时逆转录聚合酶链反应、蛋白质免疫印迹法和免疫染色法研究NECTIN-4的表达。此外,我们使用过表达NECTIN-4的细胞进行基质胶侵袭试验和细胞毒性试验。
与正常妊娠相比,子痫前期胎盘组织中NECTIN4转录本水平升高。在半定量蛋白质免疫印迹法中,子痫前期胎盘组织中NECTIN-4蛋白水平更高。NECTIN-4定位于合体滋养层细胞的顶端细胞膜,而非黏着连接部位。在细胞滋养层细胞和蜕膜中的一部分细胞中也检测到了NECTIN-4。过表达NECTIN-4的滋养层细胞在基质中正常迁移。然而,自然杀伤(NK)细胞对过表达NECTIN-4的滋养层细胞表现出强烈的细胞毒性作用。子痫前期胎盘组织的NECTIN4基因未发现致病的基因变异。
目前尚不清楚是什么因素诱导滋养层细胞中NECTIN-4过表达,这可能通过异常的免疫反应和子痫前期妊娠的发生导致胎盘形成异常。