Table of Contents Author Guidelines Submit a Manuscript
Stem Cells International
Volume 2017, Article ID 2362630, 14 pages
Research Article

Molecular Genetic Analysis of Human Endometrial Mesenchymal Stem Cells That Survived Sublethal Heat Shock

1Institute of Cytology, Russian Academy of Sciences, Tikhoretskay Ave 4, St. Petersburg 194064, Russia
2Medical Genetics Centre Genotek, Nastavnichesky Alley 17-1-15, Moscow 10510, Russia
3Vavilov Institute of General Genetics, Russian Academy of Sciences, Gubkina Str. 3, Moscow 119333, Russia

Correspondence should be addressed to A. E. Vinogradov; ur.sarcni@nivea, O. V. Anatskaya; moc.liamg@ayakstana.aglo, and L. L. Alekseenko;

Received 20 April 2017; Accepted 13 July 2017; Published 10 December 2017

Academic Editor: Josef Buttigieg

Copyright © 2017 A. E. Vinogradov et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


High temperature is a critical environmental and personal factor. Although heat shock is a well-studied biological phenomenon, hyperthermia response of stem cells is poorly understood. Previously, we demonstrated that sublethal heat shock induced premature senescence in human endometrial mesenchymal stem cells (eMSC). This study aimed to investigate the fate of eMSC-survived sublethal heat shock (SHS) with special emphasis on their genetic stability and possible malignant transformation using methods of classic and molecular karyotyping, next-generation sequencing, and transcriptome functional analysis. G-banding revealed random chromosome breakages and aneuploidy in the SHS-treated eMSC. Molecular karyotyping found no genomic imbalance in these cells. Gene module and protein interaction network analysis of mRNA sequencing data showed that compared to untreated cells, SHS-survived progeny revealed some difference in gene expression. However, no hallmarks of cancer were found. Our data identified downregulation of oncogenic signaling, upregulation of tumor-suppressing and prosenescence signaling, induction of mismatch, and excision DNA repair. The common feature of heated eMSC is the silence of MYC, AKT1/PKB oncogenes, and hTERT telomerase. Overall, our data indicate that despite genetic instability, SHS-survived eMSC do not undergo transformation. After long-term cultivation, these cells like their unheated counterparts enter replicative senescence and die.