Journal of Systems Biology & Proteome Research

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Rapid Communication - Journal of Systems Biology & Proteome Research (2022) Volume 3, Issue 3

Proteomic study of decidua in recurrent pregnancy loss patients

Aboma Otchere*

Department of Veterinary Laboratory

*Corresponding Author:
Aboma Otchere
Department of Veterinary Laboratory
Ambo University
Guder, Ethiopia

Received:06-May-2022, Manuscript No. AASBPR-22-63479; Editor assigned: 07-May-2022, PreQC No. AASBPR-22-63479(PQ); Reviewed:20-May-2022, QC No. AASBPR-22-63479; Revised:23-May-2022, Manuscript No. AASBPR-22-63479(R); Published:30-May-2022, DOI:10.35841/aasbpr-3.3.114

Citation: Otchere A. Proteomic study of decidua in recurrent pregnancy loss patients. J Syst Biol Proteome Res. 2022;3(3):114

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The physiological process of pregnancy is complex. The complex management of the maternal–fetal interface is critical for a normal pregnancy and the prevention of foetal rejection and subsequent abortion. Previous research has focused on the clinical characteristics of foetal rejection and abortion, as well as pathological indicators. However, there has been no meaningful progress. To develop prospective therapy methods, it's crucial to understand the biological processes of Recurrent Pregnancy Loss (RPL). The goal of this research was to learn more about RPL's pathogenesis. In this work, differentially expressed proteins in decidual from RPL patients and matched normal controls were identified using relative and absolute quantification (iTRAQ) technology combined with liquid chromatography-tandem mass spectrometry (LC–MS/MS) analysis. Furthermore, overexpression of NDUFBD3 in decidual cells resulted in lower levels of mitochondrial membrane potential expression. These findings show that NDUFB3 may play a key role in the progression of RPL pathology. This extensive investigation of RPL proteomics identifies a new candidate: NDUFB3, which could be researched further to help explain RPL's pathogenic mechanism.

The maternal endometrium (decidua), the conceptus, and the placenta engage in a complicated molecular conversation to ensure a successful pregnancy. The endometrium experiences considerable cyclic biochemical and morphological changes during embryonic implantation and placental development. This is known as stromal cell decidualization, and it is necessary for the embryo to attach to and infiltrate the uterine epithelium[1].

The decidua is essential for embryonic growth and early pregnancy because it secretes fibronectin and insulin-like growth factor binding protein-1, which bind to trophoblast-specific integrins and influence trophoblast migration and invasion. A rising number of studies link human decidua malfunction to a variety of reproductive illnesses and pregnancy problems, including RPL. In the postgenomic era, proteomics, or the large-scale study of proteins, contributes significantly to our understanding of gene function[2].

Tandem Mass Tags (TMTs) are a powerful tool for proteomic analysis, allowing researchers to examine protein expression patterns in cells under a variety of healthy and pathological situations. Thus, combining proteomics with high-throughput polymorphism analysis may allow us to decipher the specific molecular complexes or pathways implicated in RPL aetiology[3]. We looked at decidua from both normal early pregnancies and recurrent pregnancy loss in this investigation. TMT sequencing was utilised to identify and characterise proteins, as well as to create distinct proteomic profiles for decidua from normal and terminated fetuses[4].

The roles of these differently expressed proteins in the maintenance of early pregnancy and the incidence of RPL were also investigated. The identification of biomarkers important for the diagnosis and prognosis of numerous disorders, including recurrent spontaneous abortion, is aided by mass spectrometry (MS)-based proteomics. The separation of intact proteins or peptides generated by trypsin treatment is the basis of MS-based proteomics[5].


We found that NDUFB3 is substantially expressed in RPL patients' decidual tissue in the current investigation. Interestingly, decidual tissue in the RPL group produced much more NDUFB3 than in the control group. Furthermore, utilising an adenovirus to overexpress NDUFB3 substantially decreased DSC outgrowth, mitochondrial membrane potential, and oxidative stress function in vitro. The relationship between elevated NDUFB3 expression and RPL provides a pathogenic criterion that can be used to diagnose and treat probable miscarriages.


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