AI Article Synopsis
- - The study investigates long-term effects of radiation therapy on heart muscle by examining microvascular density, collagen deposition, and the heat shock protein HSPA1 in mice.
- - Researchers exposed C57BL/6 mice to varying doses of X-ray radiation and analyzed heart tissues 20, 40, and 60 weeks post-irradiation.
- - Findings indicate a significant reduction in microvessel density and an increase in collagen and HSPA1 levels over time, suggesting these changes may contribute to late radiation cardiotoxicity.
Article Abstract
Purpose: Improvement of radiotherapy techniques reduces the exposure of normal tissues to ionizing radiation. However, the risk of radiation-related late effects remains elevated. In the present study, we investigated long-term effects of radiation on heart muscle morphology.
Materials And Methods: We established a mouse model to study microvascular density (MVD), deposition of collagen fibers, and changes in accumulation of heat shock 70 kDa protein 1 (HSPA1) in irradiated heart tissue. Hearts of C57BL/6 mice received a single dose of X‑ray radiation in the range 0.2-16 Gy. Analyses were performed 20, 40, and 60 weeks after irradiation.
Results: Reduction in MD was revealed as a long-term effect observed 20-60 weeks after irradiation. Moreover, a significant and dose-dependent increase in accumulation of HSPA1, both cytoplasmic and nuclear, was observed in heart tissues collected 20 weeks after irradiation. We also noticed an increase in collagen deposition in hearts treated with higher doses.
Conclusions: This study shows that some changes induced by radiation in the heart tissue, such as reduction in microvessel density, increase in collagen deposition, and accumulation of HSPA1, are observed as long-term effects which might be associated with late radiation cardiotoxicity.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5847036 | PMC |
| http://dx.doi.org/10.1007/s00066-017-1220-z | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Neuronal-specific impairment of heparan sulfate degradation in Drosophila reveals pathogenic mechanisms for Mucopolysaccharidosis type IIIA.
Exp Neurol
May 2018
Department of Genetics and Evolution, School of Biological Sciences, The University of Adelaide, Adelaide, SA 5005, Australia; Hopwood Centre for Neurobiology, South Australian Health and Medical Research Institute, PO Box 11060, Adelaide, SA 5001, Australia. Electronic address:
Mucopolysaccharidosis type IIIA (MPS IIIA) is a lysosomal storage disorder resulting from the deficit of the N-sulfoglucosamine sulfohydrolase (SGSH) enzyme that leads to accumulation of partially-degraded heparan sulfate. MPS IIIA is characterized by severe neurological symptoms, clinically presenting as Sanfilippo syndrome, for which no effective therapy is available. The lysosomal SGSH enzyme is conserved in Drosophila and we have identified increased levels of heparan sulfate in flies with ubiquitous knockdown of SGSH/CG14291.
View Article and Find Full Text PDFHeart irradiation reduces microvascular density and accumulation of HSPA1 in mice.
Strahlenther Onkol
March 2018
Department of Radiotherapy, Maria Skłodowska-Curie Memorial Cancer Center and Institute of Oncology Gliwice Branch, Wybrzeże Armii Krajowej 15, 44-101, Gliwice, Poland.
Article Synopsis
- - The study investigates long-term effects of radiation therapy on heart muscle by examining microvascular density, collagen deposition, and the heat shock protein HSPA1 in mice.
- - Researchers exposed C57BL/6 mice to varying doses of X-ray radiation and analyzed heart tissues 20, 40, and 60 weeks post-irradiation.
- - Findings indicate a significant reduction in microvessel density and an increase in collagen and HSPA1 levels over time, suggesting these changes may contribute to late radiation cardiotoxicity.
Role of the Red Ginseng in Defense against the Environmental Heat Stress in Sprague Dawley Rats.
Molecules
November 2015
Department of Food Science and Biotechnology, College of Life Science, CHA University, Kyonggi 463-400, Korea.
Global temperature change causes heat stress related disorders in humans. A constituent of red ginseng has been known the beneficial effect on the resistance to many diseases. However, the mechanism of red ginseng (RG) against heat stress still remains unclear.
View Article and Find Full Text PDFActivity of heat shock genes' promoters in thermally contrasting animal species.
PLoS One
January 2016
Engelhardt Institute of Molecular Biology RAS, Vavilov str. 32, Moscow, 119991, Russia.
Heat shock gene promoters represent a highly conserved and universal system for the rapid induction of transcription after various stressful stimuli. We chose pairs of mammalian and insect species that significantly differ in their thermoresistance and constitutive levels of Hsp70 to compare hsp promoter strength under normal conditions and after heat shock (HS). The first pair includes the HSPA1 gene promoter of camel (Camelus dromedarius) and humans.
View Article and Find Full Text PDFHeat shock preconditioning protects against ER stress-induced apoptosis through the regulation of the BH3-only protein BIM.
FEBS Open Bio
October 2014
Apoptosis Research Centre, NUI Galway, Ireland.
A mild heat shock (HS) preconditioning and acquisition of thermotolerance protects cells against a variety of cytotoxic agents that otherwise induce apoptosis. Here we tested whether there is a molecular link between HS preconditioning and endoplasmic reticulum (ER) stress-induced apoptosis. ER stress results from a loss of ER lumen homeostasis, culminating in an accumulation of unfolded/misfolded proteins in the ER and activation of unfolded protein response (UPR).
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!