Back to Search
Start Over
Deletion of Apoptosis Inhibitor of Macrophage (AIM)/CD5L Attenuates the Inflammatory Response and Infarct Size in Acute Myocardial Infarction
- Source :
- Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease
- Publication Year :
- 2016
- Publisher :
- Ovid Technologies (Wolters Kluwer Health), 2016.
-
Abstract
- Background An excessive inflammatory response after myocardial infarction (MI) increases myocardial injury. The toll‐like receptor (TLR)‐4 is activated by the recognition of endogenous ligands and is proinflammatory when there is myocardial tissue injury. The apoptosis inhibitor of the macrophage (AIM) is known to provoke an efflux of saturated free fatty acids (FFA) due to lipolysis, which causes inflammation via the TLR‐4 pathway. Therefore, this study investigated the hypothesis that AIM causes a proinflammatory response after MI. Methods and Results The left anterior descending coronary artery was ligated to induce MI in both AIM‐knockout (AIM −/− ) and wild‐type (WT) mice. After 3 days, the inflammatory response from activation of the TLR‐4/NFκB pathway was assessed, and infarct size was measured by staining with triphenyltetrazolium chloride. In addition, left ventricular remodeling was examined after 28 days. Although the area at risk was similar between AIM −/− and WT mice, the infarct size was significantly smaller in AIM −/− mice ( P =0.02). The heart weight–to–body weight ratio and myocardial fibrosis were also decreased in the AIM −/− mice, and the 28‐day survival rate was improved ( P −/− mice, myocardial IRAK4 and NFκB activity were decreased (all P P P =0.03, respectively). Furthermore, NFκB DNA‐binding activation via TLR‐4, neutrophil infiltration, and inflammatory mediators were decreased in AIM −/− mice. Conclusions The deletion of AIM reduced the inflammatory response and infarct size and improved survival after myocardial infarction.
- Subjects :
- 0301 basic medicine
medicine.medical_specialty
Blotting, Western
Myocardial Infarction
Inflammation
Fatty Acids, Nonesterified
030204 cardiovascular system & hematology
toll‐like receptor‐4
Proinflammatory cytokine
Mice
03 medical and health sciences
0302 clinical medicine
Ischemia
Internal medicine
medicine
Animals
Myocardial infarction
Receptors, Immunologic
Ventricular remodeling
Receptor
Original Research
Heart Failure
Mice, Knockout
Receptors, Scavenger
Lipids and Cholesterol
biology
business.industry
apoptosis inhibitor of macrophage
Hemodynamics
NF-kappa B
free fatty acids
IRAK4
medicine.disease
Mice, Inbred C57BL
Nitric oxide synthase
Disease Models, Animal
030104 developmental biology
Endocrinology
Animal Models of Human Disease
Echocardiography
biology.protein
Cardiology
Myocardial fibrosis
medicine.symptom
Apoptosis Regulatory Proteins
Cardiology and Cardiovascular Medicine
business
Basic Science Research
Subjects
Details
- ISSN :
- 20479980
- Volume :
- 5
- Database :
- OpenAIRE
- Journal :
- Journal of the American Heart Association
- Accession number :
- edsair.doi.dedup.....841e0f4c7a26e21ca673b5eb9bce8987