Affiliation:
1. Department of Cardiology, The Affiliated Huaian No. 1 People’s Hospital of Nanjing Medical University, Huai’an,
223300, China
2. Department of Nursing, Jiangsu College of Nursing, Huai’an, 223005, China
Abstract
Background:
Dual Specificity Phosphatase 3 (DUSP3) regulates the innate immune
response and is associated with ischemia/reperfusion (I/R). However, the precise function of
DUSP3 in acute myocardial infarction (AMI) remains to be established.
Methods:
In this study, the AMI model in vivo was established in mice by permanent left anterior
descending coronary artery (LAD) occlusion, and primary neonatal mouse cardiomyocytes were
treated with hypoxia for 12 hours to mimic AMI in vitro. Sh-DUSP3 and AAV9-sh-DUSP3 were
used to knock down the DUSP3 expression. LVEF%, LVFS%, SOD1, and HO-1 level, and TTC
staining were used to test the cardiac function. Flow cytometric analysis, Western blot, and
TUNEL staining were used to investigate the effect of DUSP3 knockdown on apoptosis. Moreover,
we detect inflammatory factors expression and oxidative stress by ELISA. Besides, we investigate
DUSP3 expression by RT-qPCR.
Results:
Our findings determined the role of DUSP3 in the progression of AMI. And demonstrated
that DUSP3 knockdown alleviated oxidative stress, inflammation, and apoptosis. In addition, our
results indicated that DUSP3 knockdown could regulate the expression of p-NF-κB, ICAM1, and
VCAM1.
Conclusion:
Our results demonstrated that the knockdown of DUSP3 could effectively alleviate
AMI symptoms and be mediated through the NF-κB signaling pathway.
Publisher
Bentham Science Publishers Ltd.
Subject
Cellular and Molecular Neuroscience,Developmental Neuroscience,Neurology,Neurology (clinical)
Cited by
3 articles.
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