Myocardial heat shock protein 60 expression is upregulated following acute cardiac rejection

Abstract Background Heat shock proteins (HSPs) are endogenous adjuvants which are upregulated following cellular injury. HSP60 may be upregulated in response to myocardial injury, inducing activation via TLR ligation on monocytes, dendritic cells and T cells. On these grounds, this study was designed to assess HSP60 expression during the rejection process following cardiac transplantation. Methods Intracellular and cell surface endomyocardial concentration of HSP60 was quantified longitudinally in a cohort of heart transplant recipients ( n = 17, 54 biopsy samples) using competitive sandwich ELISA. Results HSP 60 concentration was low before and during an acute rejection episode. Surprisingly an increase of HSP60 was observed in the period following rejection during recovery ( p = 0.026). Conclusions This novel data demonstrates that human endomyocardial HSP60 is increased following an acute rejection episode. This may occur following endomyocardial damage as a result of immune cell infiltration and graft cell damage. However, in contrast to the general assumption that this molecule represents a danger signal, our findings suggest HSP60 expression may be induced as part of a protective response following tissue damage.