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Quantitative proteomics suggest a potential link between early embryonic death and trisomy 16.

Authors :
Yao, Ting
Hou, Haiyan
Liu, Guozhong
Wu, Jun
Qin, Zhe
Sun, Yang
Jin, Xiaohan
Chen, Jun
Chen, Yaqiong
Xu, Zhongwei
Source :
Reproduction, Fertility & Development. 2019, Vol. 31 Issue 6, p1116-1126. 11p.
Publication Year :
2019

Abstract

Activation of extracellular signal-regulated kinase (ERK) signalling, alteration of the uterine microenvironment and a reduction in human chorionic gonadotrophin production have been linked with fetal trisomy 16-induced early embryonic death (EED). However, the detailed biological mechanism of EED remains unclear. Using quantitative proteomics we successfully screened differentially expressed proteins in the villous tissues from patients with EED and fetal trisomy 16 (EEDT16), patients with EED but normal fetal chromosomes (EEDNC) and patients undergoing elective abortion with normal fetal chromosomes (EANC) as the reference group. Compared with the reference group, we identified 337 and 220 differentially expressed proteins in EEDT16 patients and EEDNC patients respectively; these were involved in critical biological processes including immune response, superoxide metabolism, inflammatory responses and so on. We found that differential expression of immunological function-related molecules, such as human leukocyte antigen-g (HLA-G), HLA-C, Fc Fragment Of IgG Receptor III (FcγR III), also named CD16, interleukin 18 (IL-18) and transforming growth factor β1 (TGF-β1), might induce EED in both EEDT16 and EEDNC patients. More severe immunological dysfunction was observed in EEDT16 patients than that in EEDNC patients. Furthermore, differential expression of implantation and invasion-related molecules, such as cytochrome b-245 light chain (CYBA), neutrophil cytosol factor 2 (NCF2), Mitogen-activated protein kinase kinase kinase 4 (MAP3K4), matrix metalloproteinase 2 (MMP2), MMP9 and tumour necrosis factor α (TNF-α) might induce EED in both EEDT16 and EEDNC patients, although more severe dysfunction in the implantation and invasion ability of villous tissues was observed in EEDT16 patients. Since the detailed biological mechanism of EEDT16 remains unclear, this study used quantitative proteomics to screen differentially expressed proteins in the villous tissues from patients with EEDT16, EEDNC and EANC. Dysfunction in immunological function and in the implantation and invasion ability was observed in EEDT16 and EEDNC patients. [ABSTRACT FROM AUTHOR]

Details

Language :
English
ISSN :
10313613
Volume :
31
Issue :
6
Database :
Academic Search Index
Journal :
Reproduction, Fertility & Development
Publication Type :
Academic Journal
Accession number :
136277674
Full Text :
https://doi.org/10.1071/RD17319