IL-17A levels increase in the infarcted region of the left ventricle in a rat model of myocardial infarction
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Ana María Ávalos [1] ; Felipe A Apablaza [1] ; Mariana Quiroz [2] ; Viviana Toledo [1] ; Juan Pedro Peña [3] ; Luis Michea [3] ; Carlos E Irarrazabal [2] ; Flavio A Carrión [1] ; Fernando E Figueroa [1]
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[1] Universidad de los Andes Facultad de Medicina Laboratorio de Inmunología Celular y Molecular
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[2] Universidad de los Andes Facultad de Medicina Laboratorio de Fisiología Molecular
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[3] Universidad de Chile Instituto de Ciencias Biomédicas Laboratorio de Fisiología Integrativa
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- Localización: Biological Research, ISSN-e 0717-6287, ISSN 0716-9760, Vol. 45, Nº. 2, 2012, págs. 193-200
- Idioma: inglés
- Enlaces
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Resumen
Th17 cells, a recently described subtype of CD4+ effector lymphocytes, have been linked to cell-mediated autoimmune and inflammatory diseases as well as to cardiovascular diseases. However, the participation of IL-17A in myocardial ischemic injury has not been clearly defined. We therefore conducted the present study to evaluate IL-17A and Th17-related cytokine levels in a rat model of myocardial infarction (MI). MI was induced in male Sprague Dawley rats by coronary artery ligation. Controls were sham-operated (Sh) or non-operated (C). Blood and samples from the left ventricle (LV) were collected at weeks 1 and 4 post-MI. At week 1, MI animals exhibited increased IL-6, IL-23 and TGF-β mRNA levels with no apparent change in IL-17 mRNA or protein levels in whole LV. Only TGF-β mRNA remained elevated at week 4 post-MI. However, further analysis revealed that IL-17A mRNA and protein levels as well as IL-6 and IL-23 mRNA were indeed increased in the infarcted region, though not in the remote non infarcted region of the LV, except for IL-23 mRNA. The increased expression of IL-17A and Th17-related cytokines in the infarcted region of LV, suggests that this proinflammatory pathway might play a role in early stages of post MI cardiac remodelling.
