Overexpression of tyrosine phosphorylated proteins in reproductive tissues of polycystic ovary syndrome rats induced by letrozole

• Published in: Asian pacific journal of reproduction Vol. 9; no. 6; pp. 275 - 282
• Main Authors: Sudtida Bunsueb, Supatcharee Arun, Arada Chaiyamoon, Alexander Tsang-Hsien Wu, Sitthichai Iamsaard
• Format: Journal Article
• Language: English
• Published: Wolters Kluwer Medknow Publications 01-11-2020
• Subjects: polycystic ovary syndrome; overexpression; tyrosine phosphorylated proteins; ovary; oviduct; uterus
• DOI: 10.4103/2305-0500.298775
• EISSN: 2305-0519
• ISSN: 2305-0500

Objective: To identify the alteration of tyrosine phosphorylated protein expression in rats with polycystic ovary syndrome (PCOS). Methods: Sixteen female Sprague-Dawley rats were divided into the control and letrozole-induced PCOS groups. The oestrus cycle of rats was performed by vaginal smear. Sex hormones and morphology of the ovary, oviduct, and uterus were observed. Expressions and intensity of androgen receptor and tyrosine phosphorylated proteins of reproductive organs were investigated by Western blot. Results: Various polycysts and increased androgen receptor expression were present in the ovary of the PCOS group. The levels of follicle-stimulating hormone and testosteone were significantly higher in the PCOS group while progesterone and estradiol levels were significantly decreased as compared with the control group (P<0.05). Only the size of uterus in the PCOS group was significantly smaller than the control group. However, the density of collagen fibers observed in PCOS uterus was greater than the control group. Moreover, tyrosine phosphorylated proteins were significantly overexpressed in ovary (52, 42, and 28 kDa), oviduct (72, 56, 42, and 28 kDa), and uterus (53 and 42 kDa) of the PCOS group compared to the control group. Conclusions: Presence of tyrosine phosphorylated proteins in the ovary, oviduct and uterus suggests that overexpression of tyrosine phosphorylated proteins may be involved in potential mechanism of female infertility especially in PCOS.