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Updated: Jul 1, 2025
A Preclinical Model of Exertional Heat Stroke in Mice
Published on: July 1, 2021
The hysteresis damage of cold exposure on tissue and transcript levels in mice
Jing Zhang1, Shiwan You2, Lan Yu3
1Shihezi University College of Chemistry and Chemical Engineering, College of Pharmacy / Key Laboratory of Xinjiang Phytomedicine Resource and Utilization, Ministry of Education, Shihezi, 832002, Xinjiang, China; Xinjiang University of Science&Technology, School of Medicine, Korla, 841000, China.
Objectives:
Although cold stress-induced damage to the heart and thyroid has been reported, specific organ associations between the heart and thyroid with delayed injury mechanisms have not been investigated. In this study, we determined the damage time and transcript levels of a large number of genes in the heart and thyroid after cold exposure. Meanwhile, we analysed the relationship between heart and thyroid injury in human medical records to determine the association of delayed injury from cold exposure.
Methods:
Mice were exposed to cold stress and hysteresis injury. Gene changes at the transcriptional level were detected using high throughput sequencing technology. The most variable genes were verified at the protein level using Western Blotting and medical records were collected and analysed.
Results:
The damage was the most severe when the animals were allowed to recover to room temperature for 4 h after exposure to cold stress. During this process, STAT1 and ATF3 genes were acutely up-regulated. Analysis of human medical records showed the highest correlation between AST and T4 under cold stress (p = 0.0011).
Conclusions:
Exposure to cold increases blood level of free thyroid hormone and biomarkers of myocardial injury, as well as related mRNA levels. These changes were more pronounced after return to room temperature.
Insights
Cold exposure causes delayed heart and thyroid injury, peaking 4 hours after returning to room temperature. STAT1 and ATF3 gene expression increased, correlating with myocardial injury biomarkers and thyroid hormones.
Area of Science:
- Physiology
- Molecular Biology
- Medical Records Analysis
Background:
- Cold stress is known to induce damage to the heart and thyroid.
- Specific organ associations and delayed injury mechanisms between the heart and thyroid post-cold exposure require further investigation.
Purpose of the Study:
- To determine the time course of cold stress-induced damage in the heart and thyroid.
- To investigate gene transcript levels in these organs following cold exposure.
- To analyze the relationship between heart and thyroid injury using human medical records to understand delayed injury mechanisms.
Main Methods:
- Mice were subjected to cold stress and hysteresis injury.
- High-throughput sequencing was used to detect transcriptional changes.
- Western blotting verified key gene changes at the protein level.
- Human medical records were collected and analyzed.
Main Results:
- Maximum damage occurred 4 hours after returning to room temperature post-cold stress.
- STAT1 and ATF3 genes showed acute upregulation during this recovery period.
- Human medical records revealed a significant correlation between AST and T4 levels under cold stress (p=0.0011).
Conclusions:
- Cold exposure elevates free thyroid hormone and myocardial injury biomarkers.
- Associated mRNA levels also increase following cold stress.
- These physiological and molecular changes are exacerbated upon returning to room temperature.
