In:
BMC Physiology, Springer Science and Business Media LLC, Vol. 7, No. 1 ( 2007-12)
Abstract:
It has been reported that Toll-like receptor 4 (TLR4) deficiency reduces infarct size after myocardial ischemia/reperfusion (MI/R). However, measurement of MI/R injury was limited and did not include cardiac function . In a chronic closed-chest model we assessed whether cardiac function is preserved in TLR4-deficient mice (C3H/HeJ) following MI/R, and whether myocardial and systemic cytokine expression differed compared to wild type (WT). Results Infarct size (IS) in C3H/HeJ assessed by TTC staining after 60 min ischemia and 24h reperfusion was significantly smaller than in WT. Despite a smaller infarct size, echocardiography showed no functional difference between C3H/HeJ and WT. Left-ventricular developed pressure measured with a left-ventricular catheter was lower in C3H/HeJ (63.0 ± 4.2 mmHg vs. 77.9 ± 1.7 mmHg in WT, p 〈 0.05). Serum cytokine levels and myocardial IL-6 were higher in WT than in C3H/HeJ (p 〈 0.05). C3H/HeJ MI/R showed increased myocardial IL-1β and IL-6 expression compared to their respective shams (p 〈 0.05), indicating TLR4-independent cytokine activation due to MI/R. Conclusion These results demonstrate that, although a mutant TLR4 signaling cascade reduces myocardial IS and serum cytokine levels, it does not preserve myocardial function . The change in inflammatory response, secondary to a non-functional TLR-4 receptor, may contribute to the observed dichotomy between infarct size and function in the TLR-4 mutant mouse.
Type of Medium:
Online Resource
ISSN:
1472-6793
DOI:
10.1186/1472-6793-7-5
Language:
English
Publisher:
Springer Science and Business Media LLC
Publication Date:
2007
detail.hit.zdb_id:
2041340-3
SSG:
12
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