Role for Toll-like receptor 3 in muscle regeneration after cardiotoxin injury

Muscle Nerve. 2011 May;43(5):733-40. doi: 10.1002/mus.21959. Epub 2011 Apr 1.

Abstract

Introduction: Sterile tissue injury induces an inflammatory response involving cytokines that have crucial roles in the tissue repair that follows.

Methods: MyH3 and type 1 interferon (IFN) were assessed by qPCR after cardiotoxin (CTX)-induced muscle injury.

Results: CTX-induced injury increased expression of IFN-regulated genes, IFIT1 and MX-2, which was blocked in type 1 IFN receptor (IFNR)-deficient mice. However, IFNR-deficient mice showed no significant differences in muscle regeneration as assessed by MyH3 expression. MyH3 was significantly reduced in TLR3-deficient but not MyD88-deficient mice. TLR3-deficient mice also showed altered expression of proinflammatory cytokines, IL-6, IL-1β, and TNF-α.

Conclusions: CTX-induced muscle injury increased markers of innate immune activation, but blocking type 1 IFN signaling had no effect on muscle regeneration. Taken together, these results suggest a role for TLR3, and perhaps other innate immune signals, in the inflammatory response to CTX-induced muscle injury and consequent muscle regeneration.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cardiotoxins / toxicity*
  • Immunity, Innate / drug effects
  • Inflammation Mediators / physiology*
  • Mice
  • Mice, Knockout
  • Muscle, Skeletal / drug effects
  • Muscle, Skeletal / injuries*
  • Muscle, Skeletal / pathology*
  • Regeneration / drug effects
  • Regeneration / physiology*
  • Toll-Like Receptor 3 / physiology*

Substances

  • Cardiotoxins
  • Inflammation Mediators
  • TLR3 protein, mouse
  • Toll-Like Receptor 3