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Updated: Jun 22, 2026
Murine Myocardial Infarction Model using Permanent Ligation of Left Anterior Descending Coronary Artery
Published on: August 16, 2019
Expression of ADAM-15 in rat myocardial infarction
Ji Ke Li1, Wen Juan Du, Shu Lin Jiang
1Department of Cardiology Surgery, The Second Clinical College of Harbin Medical University, Harbin, China.
Abstract:
A disintegrin and metalloprotease-15 (ADAM-15) is a potential novel regulator of inflammatory response and tissue remodelling, which is thought to have the ability to attenuate the cardiac function resulting from myocardial infarction (MI). Therefore, the aim of our study was to investigate the expression of ADAM-15 in rat MI. Wistar rats were subjected to MI by ligation of the left anterior descending coronary artery. Euthanasia was performed at 1, 3, 7 and 14 days following MI. The mRNA and protein expression levels of ADAM-15 were detected respectively by reverse transcription-polymerase chain reaction (RT-PCR) and Western blot. The localization of ADAM-15 protein was observed by immunohistochemistry. Compared with sham-MI, the expression of ADAM-15 in MI increased at day 1, reached to maximum at day 3, decreased at day 7 and day 14 gradually. In addition, we also found that the localization of ADAM-15 was mainly at cardiac myocytes in the border area of MI and some macrophages in the border and infarcted areas. This study revealed a significant difference of ADAM-15 expression in rat MI and indicated that ADAM-15 maybe one of the important factors involved in inflammatory response and cardiac remodelling of rat MI.
Insights
Disintegrin and metalloprotease-15 (ADAM-15) expression increases after myocardial infarction (MI) in rats, peaking at 3 days. ADAM-15 is localized in cardiac myocytes and macrophages, suggesting its role in cardiac remodeling and inflammation post-MI.
Area of Science:
- Cardiovascular Biology
- Molecular Medicine
- Inflammation Research
Background:
- Myocardial infarction (MI) significantly impacts cardiac function and involves complex inflammatory and remodeling processes.
- A disintegrin and metalloprotease-15 (ADAM-15) is implicated as a regulator of inflammation and tissue repair, with potential roles in cardiac pathology.
Purpose of the Study:
- To investigate the temporal expression and localization of ADAM-15 in a rat model of myocardial infarction.
- To elucidate the potential involvement of ADAM-15 in the inflammatory response and cardiac remodeling following MI.
Main Methods:
- Myocardial infarction was induced in Wistar rats via coronary artery ligation.
- ADAM-15 mRNA and protein levels were quantified using RT-PCR and Western blot at 1, 3, 7, and 14 days post-MI.
- Immunohistochemistry was employed to determine the cellular localization of ADAM-15 protein.
Main Results:
- ADAM-15 expression was significantly upregulated in the infarcted heart compared to sham controls.
- Expression levels peaked at day 3 post-MI, followed by a gradual decrease at days 7 and 14.
- ADAM-15 protein was primarily detected in cardiac myocytes within the border zone and in macrophages in the border and infarcted areas.
Conclusions:
- ADAM-15 expression is dynamically regulated following myocardial infarction in rats.
- The localization of ADAM-15 suggests its involvement in the inflammatory cell infiltration and tissue remodeling characteristic of MI.
- ADAM-15 represents a potential therapeutic target for managing cardiac dysfunction after MI.
