SavedAdd your journal

Journals / Düzce Tıp Fakültesi Dergisi / 2026 / Volume: 28 Issue: 2

Changes in the Myometrium of Rat with Polycystic Ovary Syndrome Induced by DHEA

Meryem İlkay Karagül(Hatay Mustafa Kemal University)0000-0002-1990-2640
Zehra Demiray Asoğlu(Department of Histology and Embryology, Faculty of Medicine, Hatay Mustafa Kemal University)0000-0003-3152-3069
Ayşe Yıldırım(Department of Histology and Embryology, Faculty of Medicine, Hatay Mustafa Kemal University)0009-0000-5216-6852
Pages
—
Publication Date
2026-08-21
🏛️Bibliographic metadata and full text access for this article are provided via DergiPark.
DergiPark Record ↗
✨

AI Summary & Key Takeaways

AI Insight
⚡ TL;DR(Too Long; Didn't Read)

Further research incorporating functional contractility assays and contraction-related molecular pathways is required to clarify the mechanisms linking myometrial remodelling to impaired reproductive outcomes in PCOS.

📌 3 Key Takeaways

🎯
Objective & Hypothesis:Aim: Polycystic ovary syndrome (PCOS) is associated with impaired fertility due to both ovarian dysfunction and alterations in uterine physiology.
📊
Key Findings & Data:The aim of this study was to demonstrate the effect of PCOS on myometrium morphology and α-actin expression, which plays a role in the contraction mechanism, as well as on the ultrastructural morphology of myometrial smooth muscle cells (MSMCs).
💡
Conclusion & Impact:Further research incorporating functional contractility assays and contraction-related molecular pathways is required to clarify the mechanisms linking myometrial remodelling to impaired reproductive outcomes in PCOS.
🔬Design:Modeling & Simulation
📍Scope:Comprehensive Sample
⚙️Variables:Polycystic ovary syndrome · α-actin · myometrial smooth muscle cells

Abstract

Aim: Polycystic ovary syndrome (PCOS) is associated with impaired fertility due to both ovarian dysfunction and alterations in uterine physiology. The aim of this study was to demonstrate the effect of PCOS on myometrium morphology and α-actin expression, which plays a role in the contraction mechanism, as well as on the ultrastructural morphology of myometrial smooth muscle cells (MSMCs). Material and Methods: Twenty-one female Sprague-Dawley rats (21 days old) were divided into control, vehicle and PCOS groups (n = 7 per group). PCOS was induced in the PCOS group by subcutaneous injections of 6 mg/100 g/day of dehydroepiandrosterone (DHEA) dissolved in 0.2 ml of sesame oil for 20 days. Light microscopic analyses of uterine tissue were performed. An ultrastructural examination of MSMCs was performed using transmission electron microscopy. Results: The PCOS group exhibited elevated epithelium thickness and stromal eosinophil infiltration. Masson trichrome staining revealed significant collagen deposition between the smooth muscle bundles in the myometrium, indicating fibrotic remodelling. Immunohistochemical analysis revealed decreased α-actin expression in the PCOS group. Ultrastructurally, MSMCs in the PCOS group demonstrated enlarged perinuclear spaces, while the morphology of dense bodies remained normal. Conclusion: PCOS induces significant remodelling of the myometrium, including increased collagen deposition, vascular dilation and early ultrastructural stress changes. These findings suggest that uterine dysfunction in PCOS may be caused by subtle yet functionally significant alterations to myometrial architecture. Further research incorporating functional contractility assays and contraction-related molecular pathways is required to clarify the mechanisms linking myometrial remodelling to impaired reproductive outcomes in PCOS.

🔖

Cite This Article

Karagül, M. İ., Asoğlu, Z. D., Yıldırım, A. (2026). Changes in the Myometrium of Rat with Polycystic Ovary Syndrome Induced by DHEA. Düzce Tıp Fakültesi Dergisi, Volume: 28 Issue: 2. https://doi.org/10.18678/dtfd.1842338

📄 Full Text PDF Viewer

📄

PDF görüntüleyici hazırlanıyor...

References (34)

  1. Lakhani K, Seifalian AM, Atiomo WU, Hardiman P. Polycystic ovaries. Br J Radiol. 2002;75(889):9-16. doi:10.1259/bjr.75.889.750009.
  2. Herrera AM, McParland BE, Bienkowska A, Tait R, Paré PD, Seow CY. 'Sarcomeres' of smooth muscle: functional characteristics and ultrastructural evidence. J Cell Sci. 2005;118(Pt 11):2381-92. doi:10.1242/jcs.02368.
  3. Zhang J, Herrera AM, Paré PD, Seow CY. Dense-body aggregates as plastic structures supporting tension in smooth muscle cells. Am J Physiol Lung Cell Mol Physiol. 2010;299:L631-8. doi:10.1152/ajplung.00087.2010.
  4. Laven JS, Imani B, Eijkemans MJ, de Jong FH, Fauser BC. Absent biologically relevant associations between serum inhibin concentrations and characteristics of polycystic ovary syndrome normogonadotrophic anovulatory infertility. Hum Reprod. 2001;16:1359-64. doi:10.1093/humrep/16.7.1359.
  5. Lopes IMRS, Baracat MCP, Simões MJ, Simões RS, Baracat EC, Soares JM Jr. Endometrium in women with polycystic ovary syndrome during the window of implantation. Rev Assoc Med Bras. 2011;57(6):702-9. doi:10.1590/S0104-42302011000600020.
  6. Cakmak H, Taylor HS. Implantation failure: molecular mechanisms and clinical treatment. Hum Reprod Update. 2011;17(2):242-53. doi:10.1093/humupd/dmq037.
  7. Aguilar HN, Mitchell BF. Physiological pathways and molecular mechanisms regulating uterine contractility. Hum Reprod Update. 2010;16(6):725-44. doi:10.1093/humupd/dmq016.
  8. van Gestel I, IJland MM, Hoogland HJ, Evers JLH. Endometrial wave-like activity in the non-pregnant uterus. Hum Reprod Update. 2003;9(2):131-8. doi:10.1093/humupd/dmg011.
  9. Gunst SJ, Zhang W. Actin cytoskeletal dynamics in smooth muscle: a new paradigm for the regulation of smooth muscle contraction. Am J Physiol Cell Physiol. 2008;295(3):C576-87. doi:10.1152/ajpcell.00253.2008.
  10. Morgan KG, Gangopadhyay SS. Cross-bridge regulation by thin filament-associated proteins. J Appl Physiol. 2001;91:953-62. doi:10.1152/jappl.2001.91.2.953.
  11. Sajadi M, Noroozzadeh M, Bagheripour F, Tehrani FR. Contractions in the isolated uterus of a rat model of polycystic ovary syndrome compared to controls in adulthood. Int J Endocrinol Metab. 2018;16:e61047. doi:10.5812/ijem.63135.
  12. Mesiano S, Welsh TN. Steroid hormone control of myometrial contractility and parturition. Semin Cell Dev Biol. 2007;18(3):321-31. doi:10.1016/j.semcdb.2007.05.003.
  13. Giudice LC. Endometrium in PCOS: implantation and predisposition to endocrine cancer. Best Pract Res Clin Endocrinol Metab. 2006;20(2):235-44. doi:10.1016/j.beem.2006.03.005.
  14. Dumesic DA, Oberfield SE, Stener-Victorin E, Marshall JC, Laven JS, Legro RS. Scientific statement on the diagnostic criteria, epidemiology, pathophysiology, and molecular genetics of polycystic ovary syndrome. Endocr Rev. 2015;36(5):487-525. doi:10.1210/er.2015-1018. Harı M, Gen R, Koyuncu MB, Durukan H, Çimen MB. Polycystic ovary syndrome in adolescent period: physical, metabolic, and hormonal features. Duzce Med J. 2022;24(3):221-6. doi:10.18678/dtfd.1089043.
  15. Khatun M, Arffman RK, Lavogina D, Kangasniemi M, Laru J, Ahtikoski A, et al. Women with polycystic ovary syndrome present with altered endometrial expression of stanniocalcin-1. Biol Reprod. 2020;102(2):306-15. doi:10.1093/biolre/ioz180.
  16. Kuyucu Y, Çelik LS, Kendirlinan Ö, Tap Ö, Mete UÖ. Investigation of uterine structural changes in the experimental model of polycystic ovary syndrome and effects of vitamin D treatment: ultrastructural and immunohistochemical study. Reprod Biol. 2018;18(1):53-9. doi:10.1016/j.repbio.2018.01.002.
  17. Palomba S, Piltonen TT, Giudice LC. Endometrial function in women with polycystic ovary syndrome: a comprehensive review. Hum Reprod Update. 2021;27(3):584-618. doi:10.1093/humupd/dmaa051.
  18. Chou AJ, Bing RS, Ding DC. Endometrial atypical hyperplasia and risk of endometrial cancer. Diagnostics. 2024;14(22):2471. doi:10.3390/diagnostics14222471.
  19. Wong ASW, Lao TTH, Cheung CW, Yeung SW, Fan HL, Ng PS, et al. Reappraisal of endometrial thickness for detection of endometrial cancer in postmenopausal bleeding. BJOG. 2016;123(3):439-46. doi:10.1111/1471-0528.13342.
  20. Walters KA, Allan CM, Handelsman DJ. Rodent models for human polycystic ovary syndrome. Biol Reprod. 2012;86(5):149:1-12. doi:10.1095/biolreprod.111.097808.
  21. Mirabolghasemi G, Kamyab Z. Changes of the uterine tissue in rats with polycystic ovary syndrome induced by estradiol valerate. Int J Fertil Steril. 2017;11(1):47-55. doi:10.22074/ijfs.2016.4794.
  22. Kim JJ, Kurita T, Bulun SE. Progesterone action in endometrial cancer, endometriosis, uterine fibroids, and breast cancer. Endocr Rev. 2013;34(1):130-62. doi:10.1210/er.2012-1043.
  23. Klein Meuleman SJM, Huang Y, Mischi M, Schoot D, de Leeuw RA, Post Uiterweer ED, et al. Normalization of subendometrial peristalsis in women with a large uterine niche following laparoscopic niche repair: a prospective cohort study. Eur J Obstet Gynecol Reprod Biol. 2025;308:15-22. doi:10.1016/j.ejogrb.2025.02.033.
  24. Zhu L, Xiao L, Che HS, Li YP, Liao JT. Uterine peristalsis exerts control over fluid migration after mock embryo transfer. Hum Reprod. 2014;29(2):279-85. doi:10.1093/humrep/det429.
  25. Kuijsters NPM, Methorst WG, Kortenhorst MSQ, Rabotti C, Mischi M, Schoot BC. Uterine peristalsis and fertility: current knowledge and future perspectives: a review and meta-analysis. Reprod Biomed Online. 2017;35(1):50-71. doi:10.1016/j.rbmo.2017.03.019.
  26. Kido A, Koyama T, Kataoka M, Yamamoto A, Saga T, Turner R, et al. Physiological changes of the human uterine myometrium during menstrual cycle: preliminary evaluation using BOLD MR imaging. J Magn Reson Imaging. 2007;26(3):695-700. doi:10.1002/jmri.21061.
  27. Leonhardt H, Gull B, Kishimoto K, Kataoka M, Nilsson L, Janson PO, et al. Uterine morphology and peristalsis in women with polycystic ovary syndrome. Acta Radiol. 2012;53(10):1195-201. doi:10.1258/ar.2012.120384.
  28. Karagul MI, Yildirim A, Demiray Asoglu Z, Dogan S, Aktas S, Un I, et al. Endoplasmic reticulum stress in myometrial smooth muscle cells and spontaneous contraction changes in the uterus of dehydroepiandrosterone-induced polycystic ovary syndrome rats. Cell Biochem Biophys. 2025;83(1):893-904. doi:10.1007/s12013-024-01521-4.
  29. Li J, Jiang X, Li C, Che H, Ling L, Wei Z. Proteomic alteration of endometrial tissues during secretion in polycystic ovary syndrome may affect endometrial receptivity. Clin Proteomics. 2022;19(1):19. doi:10.1186/s12014-022-09353-1.
  30. Yang X, Xiaoping W, Nan D, Jian Z, Xiaofeng L, Liwei Y, et al. Proteomic and bioinformatic analysis of human endometrium from polycystic ovarian syndrome with and without insulin resistance. Gynecol Endocrinol. 2023;39(1):2173948. doi:10.1080/09513590.2023.2173948.
  31. Zhang J, Ding N, Xin W, Yang X, Wang F. Quantitative proteomics reveals that a prognostic signature of the endometrium of the polycystic ovary syndrome women based on ferroptosis proteins. Front Endocrinol (Lausanne). 2022;13:871945. doi:10.3389/fendo.2022.871945.
  32. Ferreira SR, Motta AB. Uterine function: from normal to polycystic ovarian syndrome alterations. Current Med Chem. 2018;25(15):1792-804. doi:10.2174/0929867325666171205144119.
  33. Amjadi F, Zandieh Z, Mehdizadeh M, Ajdary M, Aghamajidi A, Raoufi E, et al. Molecular signature of immunological mechanisms behind impaired endometrial receptivity in polycystic ovarian syndrome. Arch Endocrinol Metab. 2022;66(3):303-11. doi:10.20945/2359-3997000000476.
  34. Yan H, Wang L, Zhang G, Li N, Zhao Y, Liu J, et al. Oxidative stress and energy metabolism abnormalities in polycystic ovary syndrome: from mechanisms to therapeutic strategies. Reprod Biol Endocrinol. 2024;22(1):159. doi:10.1186/s12958-024-01337-0.