Cell and Tissue BiologyCell and Tissue BiologyЦитология0041-37713034-6061The Russian Academy of Sciences66959810.31857/S0041377124030091PEBMCKArticlesСтатьиResearch ArticleFeatures of molecular phenotype and ultrastructure of smooth muscle cells in ascending aorta in premature born ratsОсобенности молекулярного фенотипа и ультраструктуры гладких миоцитов восходящей части аорты преждевременно рожденных крысSerebryakovaO. N.СеребряковаО. Н.
Russian Federation

Department of Morphology and General Pathology

кафедра морфологии и общей патологии

oserebryakovan@gmail.comIvanovaV. V.ИвановаВ. В.
Russian Federation

Department of Morphology and General Pathology

кафедра морфологии и общей патологии

oserebryakovan@gmail.comMiltoI. V.МильтоИ. В.
Russian Federation

Department of Morphology and General Pathology, Department of Molecular and Cellular Radiobiology

кафедра морфологии и общей патологии, отдел молекулярной и клеточной радиобиологии

oserebryakovan@gmail.comSiberian State Medical UniversityСибирский государственный медицинский университетSeversk Biophysical Research Center of the FMBA of RussiaСеверский биофизический научный центр ФМБА России1505202466328929827022025Copyright ©; 2024, Russian Academy of SciencesCopyright ©; 2024, Российская академия наук2024Russian Academy of SciencesРоссийская академия наукhttps://journals.eco-vector.com/0041-3771/article/view/669598

Preterm birth can contribute to the development of diseases of circulatory system in adulthood due to the incompleteness of the morphogenesis of the blood vessels wall. Smooth muscle cells are the leading cell population in the middle shell of the aortic wall and are plastic in nature, i. e. they are able to change their phenotype depending on the conditions of their environment. The presence of synthetically active smooth muscle cells in the aortic wall of an adult individual is a predictor of the formation of a wide range of cardiovascular diseases. The aim of our study is to identify the morphofunctional features of molecular phenotype and ultrastructure of smooth muscle cells of ascending aorta wall in rats born 12 and 24 hours prematurely. The paper presents the results of immunohistochemical and morphometric, as well as ultrastructural analysis of ascending aorta wall in Wistar rats born 12 and 24 hours prematurely. It has been shown that preterm birth leads to a later change in the phenotype of smooth muscle cells from synthetic to contractile, which can negatively affect the morphofunctional state of the cardiovascular system.

Преждевременное рождение может способствовать развитию болезней системы кровообращения во взрослом возрасте в связи с незавершенностью морфогенеза стенки кровеносных сосудов. Гладкие миоциты являются ведущей клеточной популяцией в средней оболочке стенки аорты и являются пластичными по своей природе, т. е. они способны менять свой фенотип в зависимости от их микроокружения. Наличие синтетически активных гладких миоцитов в стенке аорты взрослого индивида является предиктором формирования широкого спектра сердечно-сосудистых заболеваний. Целью нашего исследования является изучение особенностей молекулярного фенотипа и ультраструктуры гладких миоцитов средней оболочки стенки восходящей части аорты крыс, рожденных на 12 и 24 ч раньше срока. В работе представлены результаты иммуногистохимического и морфометрического, а также ультраструктурного анализа стенки восходящей части аорты крыс Вистар, рожденных на 12 ч и 24 ч раньше срока. Показано, что преждевременное рождение приводит к более поздней смене фенотипа гладких миоцитов с синтетического на сократительный, что может негативно отразиться на морфофункциональном состоянии сердечно-сосудистой системы.

aortapreterm birthratsphenotypesmooth muscle cellsаортапреждевременное рождениекрысыфенотипгладкие миоцитыРоссийский Научный ФондRussian Science Foundation24-25-0001Серебрякова О.Н, Иванова В. В., Мильто И. В. 2023. Особенности строения стенки восходящей части аорты преждевременно рожденных крыс. Цитология. Т. 65. № 6. С. 593. (Serebryakova O.N, Ivanova V. V., Milto I. V. 2023. Structural features of ascending aorta wall in premature born rats. Tsitologiya. V. 65. P. 593—600.)Balint B., Bernstorff I. G., Schwab T., Schäfers H. J. 2023. Age-dependent phenotypic modulation of smooth muscle cells in the normal ascending aorta. Front. Cardiovasc. Med. V. 10: 1114355. doi: 10.3389/fcvm.2023.1114355Barnard C., Peters M., Sindler A., Farrell E., Baker K.., Palta M., Stauss H., Dagle J., Segar J., Pierce G., Eldridge M., Bates M. 2020. Increased aortic stiffness and elevated blood pressure in response to exercise in adult survivors of prematurity. Physiol. Rep. V. 8: e14462. doi: 10.14814/phy2.14462Bensley J., De Matteo R., Harding R., Black M. 2016. The effects of preterm birth and its antecedents on the cardiovascular system. Acta Obstet. Gynecol. Scand. V. 95. P. 652.Berry C., Looker T., Germain J. 1992. The growth and development of the rat aorta. J. Anat. V. 113. P. 1.Cao G., Xuan X., Hu J., Zhang R., Jin H., Dong H. 2022. How vascular smooth muscle cell phenotype switching contributes to vascular disease. Cell Commun. Signal. V. 20: 180. doi: 10.1186/s12964-022-00993-2Figueroa J., Oubre J., Vijayagopal P. 2004. Modulation of vascular smooth muscle cells proteoglycan synthesis by the extracellular matrix. J. Cell Physiol. V. 198. P. 302.Fujimoto T., Tokuyasu K. T., Singer S. J. Direct morphological demonstration of the coexistence of vimentin and desmin in the same intermediate filaments of vascular smooth muscle cells. J. Submicrosc. Cytol. 1987. V. 19. P. 1.Gabbiani G., Schmid E., Winter S., Chaponnier C., de Ckhastonay C., Vandekerckhove J., Weber K., Franke W. W. Vascular smooth muscle cells differ from other smooth muscle cells: predominance of vimentin filaments and a specific alpha-type actin. Proc. Natl. Acad. Sci. USA. 1981. V. 78. P. 298.Halayko A., Salari H., Ma X., Stephens N. 1996. Markers of airway smooth muscle cell phenotype. Am. J. Physiol. V. 270. P. 1040.Johnson R., Solanki R., Warren D. 2021. Mechanical programming of arterial smooth muscle cells in health and ageing. Biophys. Rev. V. 13. P. 757.Kanda K., Matsuda T. Mechanical stress-induced orientation and ultrastructural change of smooth muscle cells cultured in three-dimensional collagen lattices. 1994. Cell Transplant. V. 3. P. 481.Lesauskaite V., Tanganelli P., Sassi C., Neri E., Diciolla F., Ivanoviene L., Epistolato M. C., Lalinga A. V., Alessandrini C., Spina D. 2001. Smooth muscle cells of the media in the dilatative pathology of ascending thoracic aorta: morphology, immunoreactivity for osteopontin, matrix metalloproteinases, and their inhibitors. Hum. Pathol. V. 32. P. 1003.Looker T., Berry C. 1997. The growth and development of rat aorta. J. Anat. V. 113. P. 17.Merrilees M., Campbell J., Spanidis E., Campbell G. 1990. Glycosaminoglycan synthesis by smooth muscle cells of differing phenotype and their response to endothelial cell conditioned medium. Atherosclerosis. V. 81. P. 245.Osborn M., Caselitz J., Puschel K., Weber K. 1987. Intermediate filament expression in human vascular smooth muscle and in arteriosclerotic plaques. Virchows Arch. A Pathol. Anat. Histopathol. V. 411. P. 449.Petsophonsakul P., Furmanik M., Forsythe R., Dweck M., Schurink G. W., Natour E., Reutelingsperger C., Jacobs M., Mees B., Schurgers L. 2019. Role of vascular smooth muscle cell phenotypic switching and calcification in aortic aneurysm formation. Arterioscler. Thromb. Vasc. Biol. V. 39. P. 1351.Qin H., Bao J., Tang J., Xu D., Shen L. 2023. Arterial remodeling: the role of mitochondrial metabolism in vascular smooth muscle cells. Am. J. Physiol. Cell Physiol. V. 324. P. 183.Rensen S., Doevendans P., van Eys G. 2007. Regulation and characteristics of vascular smooth muscle cell phenotypic diversity. Neth. Heart J. V. 15. P. 100.Schmid E., Osborn M., Rungger-Brändle E., Gabbiani G., Weber K., Franke W. 1982. Distribution of vimentin and desmin filaments in smooth muscle tissue of mammalian and avian aorta. Exp. Cell Res. V. 137. P. 329.Shi J., Yang Y., Cheng A., Xu G., He F. 2020. Metabolism of vascular smooth muscle cells in vascular diseases. Am. J. Physiol. Heart Circ. Physiol. V. 319. P. 613.Sweeney M., Jones C., Greenwood S., Baker P., Taggart M. 2006. Ultrastructural features of smooth muscle and endothelial cells of isolated isobaric human placental and maternal arteries. Placenta. V. 27. P. 635.Tang H., Chen A., Zhang H., Gao X., Kong X., Zhang J. 2022. Vascular smooth muscle cells phenotypic switching in cardiovascular diseases. Cells. V. 11: 4060. doi: 10.3390/cells11244060Thyberg J., Nilsson J., Palmberg L., Sjölund M. 1985. Adult human arterial smooth muscle cells in primary culture. Modulation from contractile to synthetic phenotype. Cell Tissue Res. V. 239. P. 69.Wagenseil J., Mecham R. Vascular extracellular matrix and arterial mechanics. 2009. Physiol. Rev. V. 89. P. 957.Wang G., Jacquet L., Karamariti E., Xu Q. 2015. Origin and differentiation of vascular smooth muscle cells. J. Physiol. V. 14. P. 3013.Wang L., Zhang J., Fu W., Guo D., Jiang J., Wang Y. 2012. Association of smooth muscle cell phenotypes with extracellular matrix disorders in thoracic aortic dissection. J. Vasc. Surg. V. 56. P. 1698.Wilson D. 2011. Vascular smooth muscle structure and function. In: Mechanisms of vascular disease: A reference book for vascular specialists. University of Adelaide Press. P. 13.Ye G., Nesmith A., Parker K. 2014. The role of mechanotransduction on vascular smooth muscle myocytes cytoskeleton and contractile function. Anat. Rec. V. 297. P. 1758.Zhang J., Wang L., Fu W., Wang C., Guo D., Jiang J., Wang Y. 2013. Smooth muscle cell phenotypic diversity between dissected and unaffected thoracic aortic media. J. Cardiovasc. Surg. V. 54. P. 511.