Molecular Genetic Analysis of Human Endometrial Mesenchymal Stem Cells That Survived Sublethal Heat Shock.
Alexander E VinogradovM A ShilinaOlga V AnatskayaLarisa L AlekseenkoI I FridlyanskayaA KrasnenkoA KimD KorostinV IlynskyA ElmuratovO TsyganovT M GrinchukN N NikolskyPublished in: Stem cells international (2017)
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.
Keyphrases
- heat shock
- induced apoptosis
- heat stress
- mesenchymal stem cells
- endothelial cells
- copy number
- heat shock protein
- gene expression
- dna repair
- stem cells
- signaling pathway
- oxidative stress
- cell cycle arrest
- genome wide
- dna damage
- cell proliferation
- single cell
- electronic health record
- squamous cell carcinoma
- dna methylation
- high temperature
- cell death
- transcription factor
- endoplasmic reticulum stress
- poor prognosis
- bone marrow
- small molecule
- drug induced
- climate change
- rna seq
- artificial intelligence
- data analysis
- binding protein
- risk assessment
- cell therapy
- protein protein
- amino acid
- dna damage response
- life cycle
- squamous cell