Stanniocalcin-1 in the female reproductive system and pregnancy

Abstract

BACKGROUND Stanniocalcin-1 (STC-1) is a widely expressed glycoprotein hormone involved in a diverse spectrum of physiological and pathophysiological processes including angiogenesis, mineral homeostasis, cell proliferation, inflammation and apoptosis. Over the last 20 years, numerous studies have reported STC-1 expression within female reproductive tissues including the uterus, ovaries and placenta and implicated STC-1 in processes such as ovarian follicular development, blastocyst implantation, vascular remodelling in early pregnancy and placental development. Notably, dysregulation of STC-1 within reproductive tissues has been linked to the onset of severe reproductive disorders including endometriosis, polycystic ovary syndrome, poor trophoblast invasion and placental perfusion in early pregnancy. Furthermore, significant changes in tissue expression and in maternal systemic concentration take place throughout pregnancy and further substantiate the vital role of this protein in reproductive health and disease. OBJECTIVE AND RATIONALE Our aim is to provide a comprehensive overview of the existing literature, to summarise the expression profile and roles of STC-1 within the female reproductive system and its associated pathologies. We highlight the gaps in the current knowledge and suggest potential avenues for future research. SEARCH METHODS Relevant studies were identified through searching the PubMed database using the following search terms: ‘stanniocalcin-1’, ‘placenta’, ‘ovary’, ‘endometrium’, ‘pregnancy’, ‘reproduction’, ‘early gestation’. Only English language papers published between 1995 and 2020 were included. OUTCOMES This review provides compelling evidence of the vital function that STC-1 plays within the female reproductive system. The literature presented summarise the wide expression profile of STC-1 within female reproductive organs, as well as highlighting the putative roles of STC-1 in various functions in the reproductive system. Moreover, the observed link between altered STC-1 expression and the onset of various reproductive pathologies is presented, including those in pregnancy whose aetiology occurs in the first trimester. This summary emphasises the requirement for further studies on the mechanisms underlying the regulation of STC-1 expression and function. WIDER IMPLICATIONS STC-1 is a pleiotropic hormone involved in the regulation of a number of important biological functions needed to maintain female reproductive health. There is also growing evidence that dysregulation of STC-1 is implicated in common reproductive and obstetric disorders. Greater understanding of the physiology and biochemistry of STC-1 within the field may therefore identify possible targets for therapeutic intervention and/or diagnosis.

Quantitative Proteomics Reveals That a Prognostic Signature of the Endometrium of the Polycystic Ovary Syndrome Women Based on Ferroptosis Proteins

“…PCOS patients’ impaired endometrial receptivity and reproductive outcomes may be affected by changes in numerous signal pathways as the disease progresses ( 17 , 42 , 43 ). In our study, the DEPs were shown to be involved in ferroptosis and mitochondrial dysfunction based on the KEGG pathway and subcellular location prediction system.…”

Chemerin Effect on the Endometrial Proteome of the Domestic Pig during Implantation Obtained by LC-MS/MS Analysis

“…Stanniocalcin 1 (STC1) is a glycoprotein assigned to the ‘regulation of cell migration’ category (GO:0030334), that reduces calcium levels and increases phosphate levels in the cells and tissues. STC1 is involved in many processes, including angiogenesis, mineral homeostasis, cell proliferation, inflammation, and apoptosis [ 37 , 38 ]. In our experiment, CHEM increased the level of this protein.…”

Transcriptomic analysis shows that surgical treatment is likely to influence the endometrial receptivity of patients with stage III/IV endometriosis

“…The transcription level of CLDN4 is significantly higher in the endometrium of idiopathic infertility and minimal endometriosis, indicating that CLDN4 overexpression might be negatively linked to endometrial receptivity ( 25 ). STC1 serves in many processes ( 26 ), and it correlates with receptivity markers during the window of implantation ( 27 ). In patients with endometriosis, STC1 is upregulated in the mid-secretary eutopic endometrium ( 28 ).…”