Alterations in Mitogen-Activated Protein Kinase Kinase and Extracellular Regulated Kinase Signaling in Theca Cells Contribute to Excessive Androgen Production in Polycystic Ovary Syndrome
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We have investigated the involvement of the MAPK signaling pathway in increased androgen biosynthesis and CYP17 gene expression in women with polycystic ovary syndrome (PCOS). A comparison of MAPK kinase (MEK1/2) and ERK1/2 phosphorylation in propagated normal and PCOS theca cells, revealed that MEK1/2 phosphorylation was decreased more than 70%, and ERK1/2 phosphorylation was reduced 50% in PCOS cells as compared with normal cells. Infection with dominant-negative MEK1 increased CYP17 mRNA and dehydroepiandrosterone (DHEA) abundance, whereas constitutively active MEK1 reduced DHEA production and CYP17 mRNA abundance. Similarly, the MEK inhibitor, PD98059, increased CYP17 mRNA accumulation and CYP17 promoter activity to levels observed in PCOS cells. Remarkably, in theca cells maintained in the complete absence of insulin, ERK1/2 phosphorylation was decreased in PCOS theca cells as compared with normal theca cells, and CYP17 mRNA and DHEA synthesis were increased in PCOS theca cells. These studies demonstrate that in PCOS cells reduced levels of activated MEK1/2 and ERK1/2 are correlated with increased androgen production, irrespective of the insulin concentration. These findings implicate alterations in the MAPK pathway in the pathogenesis of excessive ovarian androgen production in PCOS.
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Insulin directly stimulates androgen production from ovaries, enhancing the activity of CYP17α and other steroidogenic enzymes with increased androgen production.
“Insulin in fact directly stimulates androgen production from ovaries, enhancing the activity of CYP17α and other steroidogenic enzymes with increased androgen production.”
From From Prediabetes to Type 2 Diabetes Mellitus in Women with Polycystic Ovary Syndrome: Lifestyle and Pharmacological Management (2020) · cites this paper as [23]
Insulin inhibits hepatic synthesis of SHBG and secretion of IGFBP-1, resulting in elevated levels of free IGF and androgens.
“It also inhibits the hepatic synthesis of SHBG and the secretion of the insulin-like growth factor-binding protein (IGFBP-1) resulting in elevated levels of free IGF and androgens.”
From From Prediabetes to Type 2 Diabetes Mellitus in Women with Polycystic Ovary Syndrome: Lifestyle and Pharmacological Management (2020) · cites this paper as [23]
At the pituitary level, insulin stimulates LH secretion, which, in association with insulin itself, acts synergistically on theca cells, increasing androgen biosynthesis.
“Furthermore, at pituitary level, insulin stimulates LH secretion, which, in association with insulin itself, acts synergistically on theca cells, increasing androgen biosynthesis [4, 23].”
From From Prediabetes to Type 2 Diabetes Mellitus in Women with Polycystic Ovary Syndrome: Lifestyle and Pharmacological Management (2020) · cites this paper as [23]
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Self-citation
- Authors
- Nelson-Degrave, V. L., Wickenheisser, J. K., Hendricks, K. L., Asano, T., Fujishiro, M., Legro, R. S., Kimball, S. R., Strauss, J. F., & McAllister, J. M.
- Affiliations
- Departments of Cellular and Molecular Physiology (V.L.N.-D., J.K.W., K.L.H., S.R.K., J.M.M.), Pennsylvania 17033;
- The University of Tokyo (JP)
- Pennsylvania State University (US)
- University of Pennsylvania (US)
- Corresponding author
- McAllister, Jan M.
- Venue
- Molecular Endocrinology
- Publisher
- The Endocrine Society
- Published
- 2005-02-01
- Volume
- 19
- Issue
- 2
- Pages
- 379-390
- ISSN
- 0888-8809 (ISSN-L)
- 1944-9917
- OpenAlex
- W2090445204
- Cited by
- 167
- References
- 70
- Citations by year
- 2026: 2 · 2025: 9 · 2024: 3 · 2023: 7 · 2022: 10 · 2021: 10 · 2020: 7 · 2019: 9 · 2018: 8 · 2017: 7 · 2016: 10 · 2015: 9 · 2014: 11 · 2013: 7 · 2012: 9
- FWCI
- 8.12
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Molecular Endocrinology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- University of Cincinnati
- National Institutes of Health
- Penn State College of Medicine
- Eunice Kennedy Shriver National Institute of Child Health and Human Development (HD-34449, R01HD033852, HD 33852, U54HD034449)
- Topics
- Health Sciences › Medicine › Reproductive Medicine › Ovarian function and disorders
- Health Sciences › Medicine › Public Health, Environmental and Occupational Health › Reproductive Biology and Fertility
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetic and Kidney Cyst Diseases
- Keywords
- polycystic ovary syndrome, theca cells, androgen production, MAPK signaling, MEK1/2, ERK1/2 phosphorylation, CYP17, dehydroepiandrosterone, PD98059, ovarian steroidogenesis
- MeSH terms
- Adenoviridae, Androgens, Animals, Cell Line, Cells, Cultured, Dehydroepiandrosterone, Dose-Response Relationship, Drug, Enzyme Inhibitors, Female, Flavonoids, Genes, Dominant, Humans, Insulin, Lac Operon, Mutation, Ovary, Phosphorylation, Polycystic Ovary Syndrome, Promoter Regions, Genetic, RNA, Messenger, Steroid 17-alpha-Hydroxylase, Steroids, Theca Cells, Time Factors, Transfection, Blotting, Western, Mitogen-Activated Protein Kinase Kinases, Extracellular Signal-Regulated MAP Kinases
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