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Upregulation of α‐enolase in acute rejection of cardiac transplant in rat model: Implications for the secretion of interleukin‐17
Author(s) -
Shi Jiahai,
Li Yangcheng,
Yang Xuechao,
Yang Dunpeng,
Zhang Yinghui,
Liu Yonghua
Publication year - 2014
Publication title -
pediatric transplantation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.457
H-Index - 69
eISSN - 1399-3046
pISSN - 1397-3142
DOI - 10.1111/petr.12306
Subject(s) - medicine , isograft , transplantation , immunosuppression , enolase , heart transplantation , immune system , immunology , immunohistochemistry , pathology
Acute allograft rejection remains a major problem in solid organ transplantation. The enzyme α‐enolase has been shown to induce an immune response in cardiac transplantation. In this study, we investigated the role of α‐enolase in acute allograft rejection in a rat model of heart transplantation. Hearts from either ( WF : RT 1 u ) or (Lew: RT 1 1 ) rats were transplanted into (Lew: RT 1 1 ) rats. No rejection occurred in the isograft group, for which the median survival time was >168 days, whereas the median survival time of the allograft group was significantly less at 10 ± 2.1 days (n = 8 per group, p < 0.001). Increased inflammation was observed in allografts, including increased α‐enolase expression and increased numbers of infiltrating CD 4 + T cells (p < 0.05). By immunohistochemical staining, we confirmed that α‐enolase was expressed not only in myocardial cells but also in the infiltrating lymphocytes. However, on the fifth day after transplantation, α‐enolase expression was no longer observed in the lymphocytes (n = 3, p < 0.001). In contrast, no lymphocytes were found in isografts after transplantation (n = 3, p < 0.001). α‐enolase expression was increased in lymphocytes, which are implicated in the acute rejection of cardiac transplants. Intragraft α‐enolase inhibition may be useful as an adjuvant therapy to systemic immunosuppression in heart transplantation.

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