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Published on: August 16, 2019
[Expression of Toll-like receptor 2/4 mRNA in myocardium in mice with hemorrhagic shock]
Tao Hang1, Shi-sen Jiang, Jian-bin Gong
1Department of Cardiology, Nanjing General Hospital of Nanjing Command, Nanjing 210002, Jiangsu, China. njht1976@yahoo.com.cn
Objective:
To investigate the effect of hemorrhagic shock without resuscitation on expression of Toll-like receptor (TLR) in myocardium of rats and its significance.
Methods:
Forty-five C57BL/6 mice were randomly divided into 3 groups: hemorrhagic group, sham operation group and lipopolysaccharide (LPS) group, with 15 mice in each group. The hemorrhagic shock mouse model was reproduced by heart puncture. Expression levels of TLR2 mRNA and TLR4 mRNA were determined by reverse transcription-polymerase chain reaction (RT-PCR). Left ventricular end-systolic pressure (LVESP) was determined and adopted as an index of left ventricle contractile function.
Results:
(1)Both hemorrhagic shock and LPS challenge led to a reduction in arterial blood pressure in mice when compared with sham operation group. Both hemorrhagic shock and LPS challenge could result in left ventricle contractile dysfunction when compared with sham operation group. (2)Expression levels for TLR2 and TLR4 genes were upregulated in myocardium to various extents after hemorrhagic shock and LPS challenge, while in contrast the changes were absent in sham operation group.
Conclusion:
(1)The up-regulation of TLR2 and TLR4 genes is closely related with hemorrhagic shock and LPS-induced left ventricle contractile dysfunction, and there may exist a difference in signal transduction pathway between the two pathological conditions. (2)The host ability of innate immune response may be reinforced by the up-regulation of TLR2 and TLR4, whereas overexpression of them may also impair the function of tissues or organs.
Insights
Hemorrhagic shock upregulates Toll-like receptors (TLR2 and TLR4) in the heart, contributing to left ventricle dysfunction. This innate immune response may be a double-edged sword, potentially harming tissues with overexpression.
Area of Science:
- Cardiovascular Physiology
- Immunology
- Molecular Biology
Context:
- Hemorrhagic shock, a critical condition, can lead to organ dysfunction.
- Toll-like receptors (TLRs) are key components of the innate immune system.
- The role of TLRs in myocardial response to shock is not fully understood.
Purpose:
- To investigate the impact of hemorrhagic shock without resuscitation on myocardial Toll-like receptor (TLR) expression in rats.
- To determine the significance of TLR expression changes in the context of hemorrhagic shock-induced cardiac dysfunction.
Summary:
- Hemorrhagic shock and lipopolysaccharide (LPS) challenge both decreased arterial blood pressure and induced left ventricle contractile dysfunction in mice compared to sham controls.
- Expression of Toll-like receptor 2 (TLR2) and Toll-like receptor 4 (TLR4) genes was significantly upregulated in the myocardium following hemorrhagic shock and LPS challenge.
- Reverse transcription-polymerase chain reaction (RT-PCR) and left ventricular end-systolic pressure (LVESP) measurements were used to assess gene expression and cardiac function.
Impact:
- Upregulation of TLR2 and TLR4 is closely linked to hemorrhagic shock and LPS-induced left ventricle contractile dysfunction.
- The observed TLR upregulation may enhance the host's innate immune response but could also impair tissue function if overexpressed.
- Findings suggest a potential therapeutic target for managing cardiac dysfunction in shock states.
