Hyperglycosylated-hCG: Its Role in Trophoblast Invasion and Intrauterine Growth Restriction

Author:

Herghelegiu Catalin Gabriel1ORCID,Veduta Alina2ORCID,Stefan Miruna Florina3,Magda Stefania Lucia34ORCID,Ionascu Iuliana5,Radoi Viorica Elena6,Oprescu Daniela Nuti17,Calin Alina Mihaela8

Affiliation:

1. Institutul National pentru Sanatatea Mamei si a Copilului “Alessandrescu Rusescu”, 020395 Bucharest, Romania

2. Filantropia Hospital, 011171 Bucharest, Romania

3. Department of Cardiology, University and Emergency Hospital, 050098 Bucharest, Romania

4. Department of Cardiology and Cardiovascular Surgery, University of Medicine and Pharmacy Carol Davila, 020021 Bucharest, Romania

5. Faculty of Veterinary Medicine, University of Agronomical Sciences and Veterinary Medicine, 011464 Bucharest, Romania

6. Department of Genetics, University of Medicine and Pharmacy Carol Davila, 020021 Bucharest, Romania

7. Department of Obstetrics and Gynecology, University of Medicine and Pharmacy Carol Davila, 020021 Bucharest, Romania

8. Medicine and Pharmacy Faculty, Dunarea de Jos University, 800008 Galati, Romania

Abstract

Human chorionic gonadotropin (hCG) is produced by the placenta and its roles have been studied for over a century, being the first known pregnancy-related protein. Although its main role is to stimulate the production of progesterone by corpus luteal cells, hCG does not represent just one biologically active molecule, but a group of at least five variants, produced by different cells and each with different functions. The hyperglycosylated variant of hCG (H-hCG) plays a key role in trophoblast invasion, placental development and fetal growth. During trophoblast invasion, H-hCG promotes extravillous cytotrophoblast cells to infiltrate the decidua, and also to colonize and remodel the spiral arteries in to low resistance, larger-diameter vessels. As fetal growth is heavily reliant on nutrient availability, impaired trophoblast invasion and remodeling of the uterine arteries, leads to a defective perfusion of the placenta and fetal growth restriction. Understanding the function of H-hCG in the evolution of the placenta might unveil new ways to manage and treat fetal growth restriction.

Publisher

MDPI AG

Subject

General Medicine

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