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Comprehensive assessment the expression of core elements related to IGFIR/PI3K pathway in granulosa cells of women with polycystic ovary syndrome.
Eur J Obstet Gynecol Reprod Biol. 2019 Feb; 233:134-140.EJ

Abstract

OBJECTIVE

Polycystic ovary syndrome (PCOS) is the most common multisystem endocrinopathy in women, characterized by chronic hyperandrogenism, ovulatory dysfunction, and polycystic ovaries. But its etiology remains elusive. A plethora of information suggests phosphatidylinositol-3-kinase (PI3K) pathway is key to the pathogenesis of PCOS but little is known about the expression pattern and possible role of insulin like growth factor 1 receptor (IGFIR)/PI3K pathway in PCOS. The goal of this study was to determine whether the core elements of the IGF1R/PI3K pathway were differentially expressed in GCs isolated from PCOS.

STUDY DESIGN

Western blot (WB) and reverse transcription-polymerase chain reaction (RT-PCR) for IGF1R, insulin receptor substrate 1 (IRS1), insulin receptor substrate 2 (IRS2) and phosphatase and tensin homolog (PTEN) related to IGFIR/PI3K pathway were performed in GCs isolated from 60 PCOS patients and 60 controls.

RESULTS

Compared to controls, body mass index (BMI), the levels of fasting plasma glucose (FPG), fasting insulin (FINS), anti-Mullerian hormone (AMH), testosterone (T), luteotropic hormone (LH), homeostasis model assessment of insulin resistance (HOMA-IR), antral follicle count (AFC) were markedly elevated while follicle stimulating hormone (FSH) decreased (p < 0.05). Furthermore, at both mRNA and protein levels, the expression of IGF1R, IRS1, IRS2 were significantly increased whereas PTEN was dramatically decreased in PCOS patients (p < 0.05).

CONCLUSION

Our findings indicate that IGFIR/PI3K pathway is differently expressed in PCOS GCs compared with controls, with IGFIR, IRS1, IRS2 significantly increased while PTEN decreased. Thus, our study probably provides new evidences about the pathogenesis of PCOS in term of molecular mechanism.

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Publisher Full Text (DOI)

Authors+Show Affiliations

He T
Center for Reproductive Medicine, Shandong University, China; National Research Center for Assisted Reproductive Technology and Reproductive Genetics, China; The Key Laboratory of Reproductive Endocrinology (Shandong University), Ministry of Education, China; Shandong Provincial Clinical Medicine Research Center for Reproductive Health, Jinan, 250100, China.
Liu Y
Department of OB&GYN, Qilu Hospital of Shandong University, Jinan, 250012, China.
Zhao S
Center for Reproductive Medicine, Shandong University, China; National Research Center for Assisted Reproductive Technology and Reproductive Genetics, China; The Key Laboratory of Reproductive Endocrinology (Shandong University), Ministry of Education, China; Shandong Provincial Clinical Medicine Research Center for Reproductive Health, Jinan, 250100, China.
Liu H
Center for Reproductive Medicine, Shandong University, China; National Research Center for Assisted Reproductive Technology and Reproductive Genetics, China; The Key Laboratory of Reproductive Endocrinology (Shandong University), Ministry of Education, China; Shandong Provincial Clinical Medicine Research Center for Reproductive Health, Jinan, 250100, China; CUHK-SDU Joint Laboratory on Reproductive Genetics, School of Biomedical Sciences, The Chinese University of Hong Kong, Hong Kong, China.
Wang Z
Center for Reproductive Medicine, Shandong University, China; National Research Center for Assisted Reproductive Technology and Reproductive Genetics, China; The Key Laboratory of Reproductive Endocrinology (Shandong University), Ministry of Education, China; Shandong Provincial Clinical Medicine Research Center for Reproductive Health, Jinan, 250100, China.
Shi Y
Center for Reproductive Medicine, Shandong University, China; National Research Center for Assisted Reproductive Technology and Reproductive Genetics, China; The Key Laboratory of Reproductive Endocrinology (Shandong University), Ministry of Education, China; Shandong Provincial Clinical Medicine Research Center for Reproductive Health, Jinan, 250100, China. Electronic address: shiyuhua2003@126.com.

MeSH

AdultBlotting, WesternCase-Control StudiesFemaleFollicular FluidGene ExpressionGranulosa CellsHumansOvulation InductionPhosphatidylinositol 3-KinasesPolycystic Ovary SyndromeRNA, MessengerReceptor, IGF Type 1Receptors, SomatomedinReverse Transcriptase Polymerase Chain ReactionSignal Transduction

Pub Type(s)

Journal Article

Language

eng

PubMed ID

30594023

Citation

He, Tingting, et al. "Comprehensive Assessment the Expression of Core Elements Related to IGFIR/PI3K Pathway in Granulosa Cells of Women With Polycystic Ovary Syndrome." European Journal of Obstetrics, Gynecology, and Reproductive Biology, vol. 233, 2019, pp. 134-140.
He T, Liu Y, Zhao S, et al. Comprehensive assessment the expression of core elements related to IGFIR/PI3K pathway in granulosa cells of women with polycystic ovary syndrome. Eur J Obstet Gynecol Reprod Biol. 2019;233:134-140.
He, T., Liu, Y., Zhao, S., Liu, H., Wang, Z., & Shi, Y. (2019). Comprehensive assessment the expression of core elements related to IGFIR/PI3K pathway in granulosa cells of women with polycystic ovary syndrome. European Journal of Obstetrics, Gynecology, and Reproductive Biology, 233, 134-140. https://doi.org/10.1016/j.ejogrb.2018.12.010
He T, et al. Comprehensive Assessment the Expression of Core Elements Related to IGFIR/PI3K Pathway in Granulosa Cells of Women With Polycystic Ovary Syndrome. Eur J Obstet Gynecol Reprod Biol. 2019;233:134-140. PubMed PMID: 30594023.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Comprehensive assessment the expression of core elements related to IGFIR/PI3K pathway in granulosa cells of women with polycystic ovary syndrome. AU - He,Tingting, AU - Liu,Yuan, AU - Zhao,Shigang, AU - Liu,Hongbin, AU - Wang,Ze, AU - Shi,Yuhua, Y1 - 2018/12/14/ PY - 2018/07/14/received PY - 2018/12/04/revised PY - 2018/12/07/accepted PY - 2018/12/30/pubmed PY - 2019/5/31/medline PY - 2018/12/30/entrez KW - Granulosa cells KW - IGF1R/PI3K pathway KW - Polycystic ovary syndrome KW - Proliferation SP - 134 EP - 140 JF - European journal of obstetrics, gynecology, and reproductive biology JO - Eur J Obstet Gynecol Reprod Biol VL - 233 N2 - OBJECTIVE: Polycystic ovary syndrome (PCOS) is the most common multisystem endocrinopathy in women, characterized by chronic hyperandrogenism, ovulatory dysfunction, and polycystic ovaries. But its etiology remains elusive. A plethora of information suggests phosphatidylinositol-3-kinase (PI3K) pathway is key to the pathogenesis of PCOS but little is known about the expression pattern and possible role of insulin like growth factor 1 receptor (IGFIR)/PI3K pathway in PCOS. The goal of this study was to determine whether the core elements of the IGF1R/PI3K pathway were differentially expressed in GCs isolated from PCOS. STUDY DESIGN: Western blot (WB) and reverse transcription-polymerase chain reaction (RT-PCR) for IGF1R, insulin receptor substrate 1 (IRS1), insulin receptor substrate 2 (IRS2) and phosphatase and tensin homolog (PTEN) related to IGFIR/PI3K pathway were performed in GCs isolated from 60 PCOS patients and 60 controls. RESULTS: Compared to controls, body mass index (BMI), the levels of fasting plasma glucose (FPG), fasting insulin (FINS), anti-Mullerian hormone (AMH), testosterone (T), luteotropic hormone (LH), homeostasis model assessment of insulin resistance (HOMA-IR), antral follicle count (AFC) were markedly elevated while follicle stimulating hormone (FSH) decreased (p < 0.05). Furthermore, at both mRNA and protein levels, the expression of IGF1R, IRS1, IRS2 were significantly increased whereas PTEN was dramatically decreased in PCOS patients (p < 0.05). CONCLUSION: Our findings indicate that IGFIR/PI3K pathway is differently expressed in PCOS GCs compared with controls, with IGFIR, IRS1, IRS2 significantly increased while PTEN decreased. Thus, our study probably provides new evidences about the pathogenesis of PCOS in term of molecular mechanism. SN - 1872-7654 UR - https://www.unboundmedicine.com/medline/citation/30594023/Comprehensive_assessment_the_expression_of_core_elements_related_to_IGFIR/PI3K_pathway_in_granulosa_cells_of_women_with_polycystic_ovary_syndrome_ DB - PRIME DP - Unbound Medicine ER -