The DOI matches its Crossref record; 36 of the 36 references it cites were found in a registry or an index.
Interleukin-17A Contributes to Myocardial Ischemia/Reperfusion Injury by Regulating Cardiomyocyte Apoptosis and Neutrophil Infiltration
Open accessAbstract
Objective This study tested whether IL-17A is involved in the pathogenesis of mouse myocardial ischemia-reperfusion (I/R) injury and investigated the mechanisms. Background Inflammatory processes play a major role in myocardial I/R injury. We recently identified interleukin (IL)-17A as an important cytokine in inflammatory cardiovascular diseases such as atherosclerosis and viral myocarditis. However, its role in myocardial I/R injury remains unknown. Methods The involvement of IL-17A was assessed in functional assays in mouse myocardial I/R injury by neutralization/repletion or genetically deficiency of IL-17A, and its mechanism on cardiomyocyte apoptosis and neutrophil infiltration were further studied in vivo and in vitro. Results IL-17A was elevated following murine left coronary artery ligation and reperfusion. Intracellular cytokine staining revealed that γδT lymphocytes, but not CD4+ helper T cells, were a major source of IL-17A. Anti-IL-17A mAb treatment or IL-17A knockout markedly ameliorated I/R injury, as demonstrated by reduced infarct size, reduced cardiac troponin T levels and improved cardiac function. This improvement was associated with a reduction in cardiomyocyte apoptosis and neutrophil infiltration. On the contrary, repletion of exogenous IL-17A induced the opposite effect. In vitro study showed that IL-17A mediated cardiomyocyte apoptosis through regulating the Bax/Bcl-2 ratio, induced CXC chemokine-mediated neutrophil migration and promoted neutrophil-endothelial cell adherence through induction of endothelial cell E-selectin and inter-cellular adhesion molecule (ICAM)-1 expression. Conclusions IL-17A mainly produced by γδT cells plays a pathogenic role in myocardial I/R injury by inducing cardiomyocyte apoptosis and neutrophil infiltration.
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Cited by
Role of Lymphocytes in Myocardial Injury, Healing, and Remodeling After Myocardial Infarction
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Self-citationCardiac fibroblasts mediate IL-17A–driven inflammatory dilated cardiomyopathy
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Metadata
- Authors
- Liao, Y.-H., Xia, N., Zhou, S.-F., Tang, T.-T., Yan, X.-X., Lv, B.-J., Nie, S.-F., Wang, J., Iwakura, Y., Xiao, H., Yuan, J., Jevallee, H., Wei, F., Shi, G.-P., & Cheng, X.
- Venue
- Journal of the American College of Cardiology
- Publisher
- Elsevier BV
- Published
- 2012-01
- Volume
- 59
- Issue
- 4
- Pages
- 420-429
- ISSN
- 0735-1097 (ISSN-L)
- OpenAlex
- W2136784260
- Cited by
- 295
- References
- 36
- FWCI
- 15.79
- Type
- journal article
- Language
- en
- Open access
- bronze
- Licence
- www.elsevier.com/tdm/userlicense/1.0/ (tdm)
- www.elsevier.com/legal/tdmrep-license (tdm)
- www.elsevier.com/open-access/userlicense/1.0/ (vor, 562 d)
- Funders
- National Basic Research Program of China
- National Natural Science Foundation of China (81170303, 30871067)
- National Institutes of Health (HL60942, HL81090, HL88547)
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- Liao, Y.-H., Xia, N., Zhou, S.-F., Tang, T.-T., Yan, X.-X., Lv, B.-J., Nie, S.-F., Wang, J., Iwakura, Y., Xiao, H., Yuan, J., Jevallee, H., Wei, F., Shi, G.-P., & Cheng, X. (2012). Interleukin-17A Contributes to Myocardial Ischemia/Reperfusion Injury by Regulating Cardiomyocyte Apoptosis and Neutrophil Infiltration. Journal of the American College of Cardiology. https://doi.org/10.1016/j.jacc.2011.10.863
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
