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

Rheumatology Section, Department of Medicine, Boston University School of Medicine, 72 East Concord Street, E501, Boston, Massachusetts 02118, USA.

Muscle & nerve 2011 May

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Sterile tissue injury induces an inflammatory response involving cytokines that have crucial roles in the tissue repair that follows. MyH3 and type 1 interferon (IFN) were assessed by qPCR after cardiotoxin (CTX)-induced muscle injury. 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. 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. Copyright © 2011 Wiley Periodicals, Inc.

Citation

Allison L Mathes, Robert Lafyatis. Role for Toll-like receptor 3 in muscle regeneration after cardiotoxin injury. Muscle & nerve. 2011 May;43(5):733-40