Expression of inhibitor of cyclindependent kinases р16ink4a in patients with endometrial hyperplasia and secondary infertility associated with external genital endometriosis and uterine myoma
- 作者: Tolibova G.H1, Tral' T.G1, Tatsiy I.D1, Kleimenova T.S1, Kvetnoy I.M1
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隶属关系:
- D.O. Ott Research Institute of Obstetrics, Gynecology and Reproductology
- 期: 卷 17, 编号 3 (2019)
- 页面: 50-53
- 栏目: Articles
- URL: https://journals.eco-vector.com/1728-2918/article/view/113101
- DOI: https://doi.org/10.29296/24999490-2019-03-09
- ID: 113101
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详细
Introduction. The endometrial hyperplasia is a current problem in connection with the high frequency in reproductiveaged patients with infertility associated with external genital endometriosis and uterine myoma. The aim ofthe study was the comparative evaluation of sex steroids expression, inflammatory markers and an inhibitor of cyclindependent kinases p16ink4a in the endometrial hyperplasia. Methods. The study included 54patients with endometrial hyperplasia. 1st group: 30patients with secondary infertility and external genital endometriosis degree I-II, 2nd group: 24patients with secondary infertility and uterine myoma (intramural and subserous form, the diameter of the nodes does not exceed of 3.0 cm). The expression of ER and PgR receptors, inflammatory markers (CD8+, CD20+, CD4+, SD138+) and inhibitor of cyclindependent kinase p16ink4a was studied by the immunohistochemical and immunofluorescent methods. Results. Patients with endometrial hyperplasia showed the same distribution of ER and PR expression in both endometrial histogenetic structures, a high incidence of chronic endometritis, and positive expression of the inhibitor of cyclindependent kinases p16ink4a in the endometrial glands and stroma. Conclusion. The high frequency of chronic endometritis and positive expression of the inhibitor of cyclindependent kinases p16ink4a in the glands and the stroma of the endometrium indicates a violation of the cell cycle of endometrial cells against the background of a chronic inflammatory process and activation of proliferative processes.
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作者简介
G. Tolibova
D.O. Ott Research Institute of Obstetrics, Gynecology and Reproductology
Email: gulyatolibova@yandex.ru
T. Tral'
D.O. Ott Research Institute of Obstetrics, Gynecology and Reproductology
I. Tatsiy
D.O. Ott Research Institute of Obstetrics, Gynecology and Reproductology
T. Kleimenova
D.O. Ott Research Institute of Obstetrics, Gynecology and Reproductology
I. Kvetnoy
D.O. Ott Research Institute of Obstetrics, Gynecology and Reproductology
参考
- Bilzer M., Roggel F., Gerbes A.L. Role of Kupffer cells in host defense and liver disease Role of Kupffer cells in host defense and liver disease. Liver International. 2006; 26: 1175-86. https://doi.org/10.111Vj.1478 3231.2006.01342.x
- You Q., Holt M., Yin H., Li G., Hu C.J., Ju C. Role of hepatic resident and infiltrating macrophages in liver repair after acute injury. Biochem. Pharmacol. 2013; 86 (6): 836-43. https://doi.org/10.10Wj. bcp.2013.07.006
- Elchaninov A.V, Fatkhudinov T.Kh., Usman N.Y, Kananykhina E.Y, Arutyunyan I.V, Makarov A.V, Lokhonina A.V, Eremina I.Z., Surovtsev V.V., Goldshtein D.V, Bolshakova G.B., Glinkina V.V., Sukhikh G.T. Dynamics of macrophage populations of the liver after subtotal hepatectomy in rats. BMC Immunol. 2018; 19 (1): 23. https://doi. org/10.1186/s12865-018-0260-1
- Лохонина А.В., Покусаев А.С., Ельчанинов А.В., Арутюнян И.В., Макаров А.В., Еремина И.З., Суровцев В.В., Большакова Г.Б., Гольдштейн Д.В., Фатхудинов Т.Х. Характеристика иммунофенотипа резидентных макрофагов печени и профиля экспрессируемых генов. Клиническая и экспериментальная морфология. 2018; 1 (25): 49-60
- Лохонина А.В., Ельчанинов А.В., Арутюнян И.В., Покусаев А.С., Макаров А.В., Еремина И.З., Суровцев В.В., Большакова Г.Б., Гольдштейн Д.В., Фатхудинов Т.Х. Морфофункциональная характеристика макрофагов эмбрионального и моноцитарного происхождения. Гены & Клетки. 2018; 2 (13): 56-62 https://doi. org/10.23868/201808020
- Martinez F.O., Gordon S. The M1 and M2 paradigm of macrophage activation: time for reassessment. F1000Prime Rep. 2014; 6: 13. https://doi.org/10.12703/P6-13
- Jablonski K.A., Amici S.A., Webb L.M., Ruiz-Rosado J.deD., Popovich P.G., Partida-Sanchez S., Guerau-de-Arellano M. Novel markers to delineate murine M1 and M2 macrophages. PLoS One. 2015; 10 (12): e0145342. https://doi.org/10.1371/journal. pone.0145342
- Epelman S., Lavine K.J., Randolph G.J. Origin and functions of tissue macrophages. Immunity. 2014; 41 (1): 21-35. https://doi. org/10.1016/j.immuni.2014.06.013
- Guilliams M., Scott C.L. Does niche competition determine the origin of tissue-resident macrophages? Nat Rev Immunol. 2017; 7: 451-60. https://doi.org/10.1038/nri.2017.42
- West M.A., Heagy W. Endotoxin tolerance: A review. Crit Care Med. 2002; 30: 64-73.
- Liu D., Cao S., Zhou Y, Xiong YJ. Recent advances in endotoxin tolerance. Cell Biochem. 2019; 120 (1): 56-70. https://doi. org/10.1002/jcb.27547
- Michalopoulos G.K. Advances in liver regeneration. Expert. Rev. Gastroenterol. Hepatol. 2014; 8 (8): 897-907. https://doi.or g/10.1586/17474124.2014.934358
- Qin H., Roberts K.L., Niyongere S.A., Cong Y, Elson C.O., Benveniste E.N. J. Immunol. 2007; 179 (9): 5966-76. Molecular mechanism of lipopolysaccharide-induced SOCS-3 gene expression in macrophages and microglia. https://doi.org/10.4049/jim-munol.179.9.5966
- Nimah M., Zhao B., Denenberg A.G., Bueno O., Molkentin J., Wong H.R., Shanley T.P. Contribution of MKP-1 regulation of p38 to endotoxin tolerance. Shock. 2005; 23 (1): 80-7. https://doi.org/10.1097/01. shk.0000145206.28812.60
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