Related Experiment Video
Updated: Jul 15, 2026
Viral Transgene Expression in Rodent Hearts and the Assessment of Cardiac Arrhythmia Risk
Published on: July 27, 2022
[Expression of integrin genes in heart of septic rat]
Zhao-cai Zhang1, Jing Yan, Guo-long Cai
1Intensive Care Unit, Zhejiang Hospital, Hangzhou 310013, China.
Insights
Sepsis alters integrin gene expression in rat hearts, with increased integrin alphaV and beta2 potentially worsening injury and decreased integrin beta1 contributing to cardiac dysfunction.
Area of Science:
- Cardiovascular Biology
- Molecular Medicine
- Sepsis Pathophysiology
Background:
- Sepsis can lead to multi-organ dysfunction, including the heart.
- The role of integrin gene expression in sepsis-induced heart injury requires further investigation.
Purpose of the Study:
- To investigate the expression profile of integrin genes in the septic rat heart.
- To elucidate mechanisms underlying sepsis-induced cardiac injury.
Main Methods:
- A cecal ligation and puncture (CLP) model was used to induce sepsis in Wistar rats.
- Hemodynamic parameters were measured using the Langendorff apparatus.
- Oligonucleotide microarrays analyzed integrin gene expression in heart tissue.
Main Results:
- Septic rat hearts showed significantly reduced cardiac output, stroke volume, and developed pressure compared to sham controls.
- Microarray analysis revealed that 20 out of 24 integrin genes were upregulated more than twofold.
- Integrin alphaV and beta2 genes were upregulated, while integrin beta1 expression was relatively insufficient.
Conclusions:
- Dysregulated integrin gene expression occurs in the septic rat heart.
- Upregulation of integrin alphaV and beta2 may exacerbate inflammatory mediator-induced heart injury.
- Insufficient expression of integrin beta1 may contribute to cardiac dysfunction during sepsis.
Objective:
To investigate the expression profile of integrin genes in heart of septic rat and relevant mechanisms responsible for sepsis-induced heart injury.
Methods:
Twelve 3-month-old male Wistar rats were randomized to 2 equal groups, sepsis model group (CLP group) undergoing ligation and perforation with needle of the distal caecum so as to establish sepsis model, and sham operation group (Sham group), undergoing sham operation only serve as controls. Twenty-four later the hearts of rats were rapidly excised. After determination of the hemodynamic parameters by using Langendorff apparatus, the isolated hearts were cut into 2 parts vertically to undergo histopathological examination and analysis of the expression of integrin genes by oligonucleotide microarrays respectively.
Results:
No overt pathological changes were detected in the hearts of septic rats, however, the cardiac output, stroke volume, heart rate, left ventricular developed pressure, left ventricular end-diastolic pressure, and maximum rate of left ventricular pressure rise of the CLP group were 29.4+/-3.3 ml/min, 0.12+/-0.01 ml, 256+/-6 bpm, 75.6+/-4.9 mm Hg, 7.5+/-0.3 mm Hg, and 2167+/-159 mm Hg/s respectively, all significantly than those of the Sham group (57.8+/-2.4 ml/min, 0.18+/-0.01 ml, 302+/-12 bpm, 90.0+/-2.7 mmHg, 8.0+/-0.3 mmHg. and 2601+/-34 mmHg/s respectively, all P<0.01). Microarray analysis showed that 20 out of 24 integrin genes were up-regulated by more than 2 times in the septic rat heart, among which the integrin alphaV and beta2 genes were upregulated and the expression of integrin beta1 gene was relatively insufficient.
Conclusion:
Maladjustment in expression of integrin genes is present in the septic rat heart. Up-regulation of integrin alphaV and beta2 genes may accelerate the heart injury mediated by inflammatory mediators, and the relatively insufficient expression of integrin beta1 gene may contribute to cardiac dysfunction.
