Key result
In a rat model of myocardial infarction, ADAM-15 expression increased at day 1, peaked at day 3, and gradually decreased at days 7 and 14 compared with sham-MI.
ADAM-15 expression is dynamically upregulated following myocardial infarction in rats, suggesting a potential role in post-MI inflammatory response and cardiac remodeling.
May implicate ADAM-15 in rat post-MI remodeling; hypothesis-generating and leaves open human translation.
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.
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Li et al. (2009) studied Myocardial infarction. Myocardial infarction (LAD ligation) vs. Sham-MI was evaluated on Expression of ADAM-15 (mRNA and protein). In a rat model of myocardial infarction, ADAM-15 expression increased at day 1, peaked at day 3, and gradually decreased at days 7 and 14 compared with sham-MI.
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