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|Title:||Leukocytic toll-like receptor 2 deficiency preserves cardiac function and reduces fibrosis in sustained pressure overload|
|Authors:||Wang J.-W. |
De Haan J.J.
De Jager S.C.A.
Van Veen T.A.B.
|Publisher:||Nature Publishing Group|
|Citation:||Wang J.-W., Fontes M.S.C., Wang X., Chong S.Y., Kessler E.L., Zhang Y.-N., De Haan J.J., Arslan F., De Jager S.C.A., Timmers L., Van Veen T.A.B., Lam C.S.P., Kleijn D.P.V.D. (2017-08-23). Leukocytic toll-like receptor 2 deficiency preserves cardiac function and reduces fibrosis in sustained pressure overload. Scientific Reports 7 (1) : 9193. ScholarBank@NUS Repository. https://doi.org/10.1038/s41598-017-09451-3|
|Abstract:||An involement of Toll-like receptor 2 (TLR2) has been established in cardiac dysfunction after acute myocardial infarction; however, its role in chronic pressure overload is unclear. We sought to evaluate the role of TLR2 in cardiac hypertrophy, fibrosis and dysfunction in sustained pressure overload. We induced pressure overload via transverse aortic constriction (TAC) in TLR2-/- and wild type (WT) mice, and followed temporal changes over 8 weeks. Despite similar increases in heart weight, left ventricular (LV) ejection fraction (EF) and diastolic function (mitral E/A ratio) were preserved in TLR2-/- mice but impaired in WT mice following TAC. TAC produced less LV fibrosis in TLR2-/- mice associated with lower mRNA levels of collagen genes (Col1a1 and Col3a1) and lower protein level of TGFbeta1, compared to WT mice. Following TAC, the influx of macrophages and CD3 T cells into LV was similar between TLR2-/- and WT mice, whereas levels of cyto/chemokines were lower in the heart and plasma in TLR2-/- mice. TLR2-/- bone marrow-derived cells protected against LVEF decline and fibrosis following TAC. Our findings show that leukocytic TLR2 deficiency protects against LV dysfunction and fibrosis probably via a reduction in inflammatory signaling in sustained pressure overload. � 2017 The Author(s).|
|Source Title:||Scientific Reports|
|Appears in Collections:||Staff Publications|
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