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Vertebrate reproductive science and technology
RESEARCH ARTICLE

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

Ting Yao https://orcid.org/0000-0001-8872-2080 A B * , Haiyan Hou C D * , Guozhong Liu E , Jun Wu F , Zhe Qin B D , Yang Sun D , Xiaohan Jin D G , Jun Chen D , Yaqiong Chen D H and Zhongwei Xu D G H
+ Author Affiliations
- Author Affiliations

A Department of Obstetrics and Gynaecology, Tianjin Nankai Hospital, No. 6 Changjiang Road, Nankai District, Tianjin 300100, China.

B Central Laboratory, Logistics University of Chinese People’s Armed Police Force, Tianjin 300309, China.

C Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100730, China.

D Department of Obstetrics and Gynaecology, Affiliated Hospital of the Chinese People’s Armed Police Force Logistics College, Tianjin 300162, China.

E Department of Obstetrics and Gynaecology, CongraMarie Women and Children’s Hospital, Tianjin 300100, China.

F Program in Public Health, Anteater Instruction & Research Bldg (AIRB) # 2034, University of California, Irvine CA 92697-3957, USA.

G Tianjin Key Laboratory of Cardiovascular Remodelling and Target Organ Injury, Pingjin Hospital Heart Centre, Tianjin 300162, China.

H Corresponding authors. Emails: xlw113@hotmail.com; chenyq82@hotmail.com

Reproduction, Fertility and Development 31(6) 1116-1126 https://doi.org/10.1071/RD17319
Submitted: 1 June 2017  Accepted: 26 January 2019   Published: 29 March 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.

Additional keywords: apoptosis, immunological dysfunction, implantation, invasion, NADPH oxidase.


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