TY - JOUR
T1 - Proteome analysis of endometrial tissue from patients with PCOS reveals proteins predicted to impact the disease
AU - Alikhani, Mehdi
AU - Amjadi, Fatemehsadat
AU - Mirzaei, Mehdi
AU - Wu, Yunqi
AU - Shekari, Faezeh
AU - Ashrafi, Mahnaz
AU - Mehdizadeh, Mehdi
AU - McKay, Matthew
AU - Taleahmad, Sara
AU - Aghajanpour, Samaneh
AU - Gupta, Vivek
AU - Baharvand, Hossein
AU - Aflatoonian, Reza
AU - Salekdeh, Ghasem Hosseini
PY - 2020/11/1
Y1 - 2020/11/1
N2 - Polycystic ovary syndrome (PCOS) is a complex disease that causes an ovulatory infertility in approximately 10% of reproductive-age women. We searched for candidate proteins that might contribute to endometrial receptivity defects in PCOS patients, and result in adverse reproductive outcomes. Shotgun proteomics approach was used to investigate the proteome profile of the endometrium at the luteal phase in PCOS patients compared to healthy fertile individuals. Biological process and pathway analyses were conducted to categorize the proteins with differential expressions. Confirmation was performed for a number of proteins via immunoblotting in new samples. 150 proteins with higher abundance, and 46 proteins with lower abundance were identified in the endometrial tissue from PCOS patients compared to healthy fertile individuals. The proteins with higher abundance were enriched in protein degradation, cell cycle, and signaling cascades. Proteins with lower abundance in PCOS patients were enriched in extracellular matrix (ECM) composition and function, as well as the salvage pathway of purine biosynthesis. Metabolism was the most affected biological process with over 100 up-regulated, and approximately 30 down-regulated proteins. Our results indicate significant imbalances in metabolism, proteasome, cell cycle, ECM related proteins, and signaling cascades in endometrial tissue of PCOS, which may contribute to poor reproductive outcomes in these patients. We postulate that the endometria in PCOS patients may not be well-differentiated and synchronized for implantation. Possible roles of the above-mentioned pathways that underlie implantation failure in PCOS will be discussed. Our findings need to be confirmed in larger populations.
AB - Polycystic ovary syndrome (PCOS) is a complex disease that causes an ovulatory infertility in approximately 10% of reproductive-age women. We searched for candidate proteins that might contribute to endometrial receptivity defects in PCOS patients, and result in adverse reproductive outcomes. Shotgun proteomics approach was used to investigate the proteome profile of the endometrium at the luteal phase in PCOS patients compared to healthy fertile individuals. Biological process and pathway analyses were conducted to categorize the proteins with differential expressions. Confirmation was performed for a number of proteins via immunoblotting in new samples. 150 proteins with higher abundance, and 46 proteins with lower abundance were identified in the endometrial tissue from PCOS patients compared to healthy fertile individuals. The proteins with higher abundance were enriched in protein degradation, cell cycle, and signaling cascades. Proteins with lower abundance in PCOS patients were enriched in extracellular matrix (ECM) composition and function, as well as the salvage pathway of purine biosynthesis. Metabolism was the most affected biological process with over 100 up-regulated, and approximately 30 down-regulated proteins. Our results indicate significant imbalances in metabolism, proteasome, cell cycle, ECM related proteins, and signaling cascades in endometrial tissue of PCOS, which may contribute to poor reproductive outcomes in these patients. We postulate that the endometria in PCOS patients may not be well-differentiated and synchronized for implantation. Possible roles of the above-mentioned pathways that underlie implantation failure in PCOS will be discussed. Our findings need to be confirmed in larger populations.
KW - Endometrial tissue
KW - Luteal phase
KW - PCOS
KW - Shotgun proteomics
UR - http://www.scopus.com/inward/record.url?scp=85093652571&partnerID=8YFLogxK
U2 - 10.1007/s11033-020-05924-3
DO - 10.1007/s11033-020-05924-3
M3 - Article
C2 - 33098551
AN - SCOPUS:85093652571
SN - 0301-4851
VL - 47
SP - 8763
EP - 8774
JO - Molecular Biology Reports
JF - Molecular Biology Reports
IS - 11
ER -