Extracellular heat shock protein 70 induces cardiomyocyte inflammation and contractile dysfunction via TLR2.

@article{Mathur2011ExtracellularHS,
  title={Extracellular heat shock protein 70 induces cardiomyocyte inflammation and contractile dysfunction via TLR2.},
  author={Sumeet Mathur and Keith R. Walley and Yingjin Wang and Toonchai Indrambarya and John H. Boyd},
  journal={Circulation journal : official journal of the Japanese Circulation Society},
  year={2011},
  volume={75 10},
  pages={2445-52}
}
BACKGROUND Toll-like receptors (TLRs) are expressed on cardiomyocytes and recognize pathogen-associated molecular patterns. Whether endogenous molecules produced by tissue injury (damage associated molecular patterns, DAMPs) can induce cardiomyocyte inflammation via TLR signalling pathways and/or reduce cardiomyocyte contractility is unknown. METHODS AND RESULTS Primary cardiomyocytes isolated from nuclear factor κ B (NFκB)-luciferase knock-in mice were used to assess NFκB signalling. DAMPs… CONTINUE READING