Immature Vascular Smooth Muscle Cells in Healthy Murine Arteries and Atherosclerotic Plaques: Localization and Activity
Autor: | Alexander Balatskiy, Ilia Ozhimalov, Maria Balatskaya, Alexandra Savina, Julia Filatova, Natalia Kalinina, Vladimir Popov, Vsevolod Tkachuk |
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Jazyk: | angličtina |
Rok vydání: | 2022 |
Předmět: |
immature smooth muscle cells
Aging Carotid Artery Common QH301-705.5 Myocytes Smooth Muscle Aorta Thoracic angiotensin II Receptor Angiotensin Type 2 Catalysis Muscle Smooth Vascular pericytes Immunophenotyping Inorganic Chemistry Cell Movement NG2 Animals Physical and Theoretical Chemistry Biology (General) atherosclerosis CD146 angiotensin II receptor type 2 Molecular Biology QD1-999 Spectroscopy Cells Cultured Cell Proliferation Mice Knockout Organic Chemistry General Medicine Arteries Plaque Atherosclerotic Computer Science Applications Mice Inbred C57BL Chemistry Stress Mechanical Shear Strength |
Zdroj: | International Journal of Molecular Sciences, Vol 23, Iss 1744, p 1744 (2022) International Journal of Molecular Sciences; Volume 23; Issue 3; Pages: 1744 |
ISSN: | 1661-6596 1422-0067 |
Popis: | The local development of atherosclerotic lesions may, at least partly, be associated with the specific cellular composition of atherosclerosis-prone regions. Previously, it was demonstrated that a small population of immature vascular smooth muscle cells (VSMCs) expressing both CD146 and neuron-glial antigen 2 is postnatally sustained in atherosclerosis-prone sites. We supposed that these cells may be involved in atherogenesis and can continuously respond to angiotensin II, which is an atherogenic factor. Using immunohistochemistry, flow cytometry, wound migration assay xCELLigence system, and calcium imaging, we studied the functional activities of immature VSMCs in vitro and in vivo. According to our data, these cells do not express nestin, CD105, and the leptin receptor. They are localized in atherosclerosis-prone regions, and their number increases with age, from 5.7% to 23%. Immature VSMCs do not migrate to low shear stress areas and atherosclerotic lesions. They also do not have any unique response to angiotensin II. Thus, despite the localization of immature VSMCs and the presence of the link between their number and age, our study did not support the hypothesis that immature VSMCs are directly involved in the formation of atherosclerotic lesions. Additional lineage tracing studies can clarify the fate of these cells during atherogenesis. |
Databáze: | OpenAIRE |
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