Stromal and Tumor Glioma-Derived Cells with Similar Characteristics have Differences in α-Smooth Muscle Actin Expression and Localization

I. Gin (Institute of Cytology, Russian Academy of Sciences, St. Petersburg, 194064, Russia)
I. Chistyakova (Institute of Cytology, Russian Academy of Sciences, St. Petersburg, 194064, Russia)
V. Zenin (Institute of Cytology, Russian Academy of Sciences, St. Petersburg, 194064, Russia)
S. Koshkin (Institute of Cytology, Russian Academy of Sciences, St. Petersburg, 194064, Russia)
A. Musorina (Institute of Cytology, Russian Academy of Sciences, St. Petersburg, 194064, Russia)
Y. Lahina (Almazov National Medical Research Centre, St. Petersburg, 197341, Russia)
G. Timin (Peter the Great Saint-Petersburg Polytechnic University, St. Petersburg, 195251, Russia)
V. Pospelov (Institute of Cytology, Russian Academy of Sciences, St. Petersburg, 194064, Russia)
S. Prikhodko (Almazov National Medical Research Centre, St. Petersburg, 197341, Russia)
A. Petukhov (Institute of Cytology, Russian Academy of Sciences, St. Petersburg, 194064, Russia; Almazov National Medical Research Centre, St. Petersburg, 197341, Russia; Scientific Technological University «Sirius», Sochi, 354340, Russia)
E. Tolkunova (Institute of Cytology, Russian Academy of Sciences, St. Petersburg, 194064, Russia)


Gliomas are solid brain tumors composed of tumor cells and recruited heterogenic stromal components. The study of the interactions between the perivascular niche and its surrounding cells is of great value in unraveling mechanisms of drug resistance in malignant gliomas. In this study, we isolated the stromal diploid cell population from oligodendroglioma and a mixed population of tumor aneuploid and stromal diploid cells from astrocytoma specimens. The stromal cells expressed neural stem/progenitor and mesenchymal markers showing the same discordant phenotype that is typical for glioma cells. Moreover, some of the stromal cells expressed CD133. For the first time, we demonstrated that this type of stromal cells had the typical myofibroblastic phenotype as the α-SMA+ cells formed α-SMA fibers and exhibited the specific function to deposit extracellular matrix (ECM) proteins at least in vitro. Immunofluorescent analysis showed diffuse or focal α-SMA staining in the cytoplasm of the astrocytoma-derived, A172, T98G, and U251MG glioma cells. We could suggest that α-SMA may be one of the main molecules, bearing protective functions. Possible mechanisms and consequences of α-SMA disruptions in gliomas are discussed.


Oligodendroglioma; Astrocytoma; Primary cell cultures; Tumor microenvironment; Myofibroblasts; Extracellular matrix

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