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Isolating, Sequencing and Analyzing Extracellular MicroRNAs from Human Mesenchymal Stem Cells
Published on: March 8, 2019
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Transcriptomic Profiling and Pathway Analysis of Mesenchymal Stem Cells Following Low Dose-Rate Radiation Exposure.
John E Slaven1, Matthew Wilkerson2,3, Anthony R Soltis2,3
1Department of Pharmacology and Molecular Therapeutics, Uniformed Services University of the Health Sciences, 4301 Jones Bridge Rd., Bethesda, MD 20814, USA.
Antioxidants (Basel, Switzerland)
|February 25, 2023
Summary
Low dose-rate radiation exposure impacts human cells differently than high doses. Chronic exposure affects metabolism and cell function, distinct from acute radiation responses, highlighting unique cellular adaptations.
Area of Science:
- Radiation Biology
- Cellular Biology
- Molecular Toxicology
Background:
- Low dose-rate radiation exposure is relevant to medical imaging, environmental factors, and space travel.
- Chronic low-dose radiation exposure is linked to Chronic Radiation Syndrome (CRS) and various health issues.
- High dose-rate radiation exposure causes acute syndromes, contrasting with chronic effects.
Purpose of the Study:
- To investigate the effects of 1-2 Gy, 0.66 cGy/h 60Co radiation on primary human mesenchymal stem cells (hMSC).
- To compare the cellular transcriptional response to low dose-rate radiation versus high dose-rate radiation.
Main Methods:
- Exposure of primary human mesenchymal stem cells (hMSC) to 1-2 Gy, 0.66 cGy/h 60Co radiation.
- Gene Ontology (GO) analysis of transcriptome changes.
- Validation using targeted qPCR and Western blotting in hMSC and human lung microvascular endothelial cells.
Main Results:
- No significant induction of apoptosis or DNA damage; continued cell proliferation observed.
- GO analysis revealed alterations in cholesterol, fatty acid, and glucose metabolism, ECM modification, cell adhesion/migration, vasoconstriction, and inflammation pathways.
- Increased hypoxia signaling and iron deficiency pathway activation, with reduced Nrf2 and related genes.
Conclusions:
- Cellular gene transcription response to low dose-rate ionizing radiation is fundamentally different from high-dose-rate exposure.
- Hypoxia and iron deficiency responses appear to be key upstream drivers of cellular adaptation to low dose-rate radiation.
- Absence of DNA damage response, cell cycle inhibition, senescence, and pro-inflammatory pathways contrasts with high dose-rate effects.
