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Journal article

Toll-like receptors 2 and 6 mediate apoptosis and inflammation in ischemic skeletal myotubes.

  • Patel H 1 Division of Surgery & Interventional Science, University College London, Royal Free Campus, London, UK.
  • Yong C 1 Division of Surgery & Interventional Science, University College London, Royal Free Campus, London, UK.
  • Navi A 1 Division of Surgery & Interventional Science, University College London, Royal Free Campus, London, UK.
  • Shaw SG 2 Department of Clinical Experimental Research, University of Bern, Bern, Switzerland.
  • Shiwen X 3 Centre for Rheumatology & Connective Tissue Disease, University College London, Royal Free Campus, London, UK.
  • Abraham D 3 Centre for Rheumatology & Connective Tissue Disease, University College London, Royal Free Campus, London, UK.
  • Baker DM 1 Division of Surgery & Interventional Science, University College London, Royal Free Campus, London, UK.
  • Tsui JC 1 Division of Surgery & Interventional Science, University College London, Royal Free Campus, London, UK.
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  • 2019-05-16
Published in:
  • Vascular medicine (London, England). - 2019
Toll-like receptors
critical limb ischemia (CLI)
inflammation
peripheral artery disease (PAD)
skeletal muscle
Aged
Animals
Apoptosis
Case-Control Studies
Cell Line
Critical Illness
Female
Humans
Inflammation Mediators
Interleukin-6
Ischemia
Male
Mice
Middle Aged
Muscle Fibers, Skeletal
Myeloid Differentiation Factor 88
NF-kappa B
Signal Transduction
Toll-Like Receptor 2
Toll-Like Receptor 6
Up-Regulation
English Critical limb ischemia (CLI) is associated with skeletal muscle damage. However, the pathophysiology of the muscle damage is poorly understood. Toll-like receptors (TLR) have been attributed to play a role in ischemia-induced tissue damage but their role in skeletal muscle damage in CLI is unknown. TLR2 and TLR6 expression was found to be upregulated in skeletal muscle of patients with CLI. In vitro, ischemia led to upregulation of TLR2 and TLR6 by myotubes, and activation of the downstream TLR signaling pathway. Ischemia-induced activation of the TLR signaling pathway led to secretion of the pro-inflammatory cytokine interleukin-6 and muscle apoptosis, which were abrogated by neutralising TLR2 and TLR6 antibodies. Our study demonstrates that TLR2 and TLR6 are upregulated in ischemic muscle and play a role in ischemia-induced muscle damage. Thus, manipulating the TLR pathway locally may be of potential therapeutic benefit.
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  • English
Open access status
green
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https://sonar.ch/global/documents/173775
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