| First Author | Paiva-Oliveira EL | Year | 2017 |
| Journal | Histochem Cell Biol | Volume | 148 |
| Issue | 1 | Pages | 49-60 |
| PubMed ID | 28293722 | Mgi Jnum | J:328165 |
| Mgi Id | MGI:6838178 | Doi | 10.1007/s00418-017-1556-6 |
| Citation | Paiva-Oliveira EL, et al. (2017) Pattern of cardiotoxin-induced muscle remodeling in distinct TLR-4 deficient mouse strains. Histochem Cell Biol 148(1):49-60 |
| abstractText | Tissue damage triggers innate immune response mediated by Toll-like receptor 4 (TLR) that recognizes endogenous host danger molecules associated with cell death and tissue inflammation, although the precise role of TLR-4 signaling in muscle tissue repair is still uncertain. Previously, we observed that TLR-4 exerted a protective effect preventing excessive muscular damage induced by Bothrops jararacussu crude venom. This study aimed to evaluate the involvement of TLR-4 at early stages of muscular tissue remodeling in distinct mouse strains after injection of purified snake venom. Muscular injury was induced by injection of 25 microl (0.05 mg/ml) of cardiotoxin (CTX) from Naja mossambica in the gastrocnemius muscle of C3H/HeN (wild-type); C3H/HeJ mice that express a non-functional TLR-4 receptor, C57BL/6 and Tlr4 (-/-) (B6 background) mice. Comparing to control, Tlr4 (-/-) mice presented at early stages (3 DPI) of muscle injury mild inflammation with low MMP-9 activity, scarce macrophage infiltration and premature change to anti-inflammatory phenotype, low TNF-alpha mRNA levels and reduced myogenin expression, with low regeneration and tissue remodeling. The presence of more Ly6C(neg) macrophages in Tlr4 (-/-) mice at 3 DPI indicates that TLR-4 may influence the differentiation into Ly6C(neg) or likely affect proliferation of such cells in the muscle. The present study shows that TLR-4 deficiency and genetic background influence the outcome of muscular tissue repair in aseptic lesions and yet still maintaining some level of signaling in the TLR4-mutant mice. |
