Expression of the genes for peroxisome proliferator-activated receptor-γ, cyclooxygenase-2, and proinflammatory cytokines in granulosa cells from women with polycystic ovary syndrome.
10.5653/cerm.2017.44.3.146
- Author:
Joong Yeup LEE
1
;
Jin Cheol TAE
;
Chung Hyon KIM
;
Doyeong HWANG
;
Ki Chul KIM
;
Chang Suk SUH
;
Seok Hyun KIM
Author Information
1. Hamchoon Women's Clinic, Seoul, Korea.
- Publication Type:Original Article
- Keywords:
Cyclooxygenase 2;
Granulosa cells;
Interleukin-6;
Peroxisome proliferator-activated receptor gamma;
Polycystic ovary syndrome;
Tumor necrosis factor-alpha
- MeSH:
Body Mass Index;
Cyclooxygenase 2*;
Cytokines*;
Embryonic Structures;
Female;
Follicle Stimulating Hormone;
Follicular Fluid;
Gene Expression;
Gonadotropins;
Granulosa Cells*;
Humans;
Interleukin-6;
Interleukins;
Luteinizing Hormone;
Oocyte Retrieval;
Oocytes;
Ovulation Induction;
Peroxisomes*;
Polycystic Ovary Syndrome*;
Polymerase Chain Reaction;
PPAR gamma;
Prostaglandin-Endoperoxide Synthases;
Reverse Transcription;
RNA, Messenger;
Sample Size;
Tumor Necrosis Factor-alpha
- From:Clinical and Experimental Reproductive Medicine
2017;44(3):146-151
- CountryRepublic of Korea
- Language:English
-
Abstract:
OBJECTIVE: To identify differences in the expression of the genes for peroxisome proliferator-activated receptor (PPAR)-γ, cyclooxygenase (COX)-2, and the proinflammatory cytokines interleukin (IL)-6 and tumor necrosis factor (TNF)-α in granulosa cells (GCs) from polycystic ovary syndrome (PCOS) patients and controls undergoing controlled ovarian stimulation. METHODS: Nine patients with PCOS and six controls were enrolled in this study. On the day of oocyte retrieval, GCs were collected from pooled follicular fluid. Total mRNA was extracted from GCs. Reverse transcription was performed and gene expression levels were quantified by realtime quantitative polymerase chain reaction. RESULTS: There were no significant differences in age, body mass index, and total gonadotropin dose, except for the ratio of luteinizing hormone to follicle-stimulating hormone between the PCOS and control groups. PPAR-γ and COX-2 mRNA was significantly downregulated in the GCs of PCOS women compared with controls (p=0.034 and p=0.018, respectively), but the expression of IL-6 and TNF-α mRNA did not show significant differences. No significant correlation was detected between the expression of these mRNA sequences and clinical characteristics, including the number of retrieved oocytes, oocyte maturity, cleavage, or the good embryo rate. Positive correlations were found among the PPAR-γ, COX-2, IL-6, and TNF-α mRNA levels. CONCLUSION: Our data may provide novel clues regarding ovarian GC dysfunction in PCOS, and indirectly provide evidence that the effect of PPAR-γ agonists in PCOS might result from alterations in the ovarian follicular environment. Further studies with a larger sample size are required to confirm these proposals.
