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Mediators of Inflammation
Volume 2017, Article ID 9450439, 11 pages
Research Article

Toll-Like Receptor 9 Promotes Survival in SERCA2a KO Heart Failure Mice

1Research Institute of Internal Medicine, Oslo University Hospital, Rikshospitalet, Oslo, Norway
2Center for Heart Failure Research, University of Oslo, Oslo, Norway
3K.G. Jebsen Inflammation Research Center, University of Oslo, Oslo, Norway
4Institute for Experimental Medical Research, Oslo University Hospital, Ullevaal, Oslo, Norway
5Bjørknes College, Oslo, Norway
6Institute for Surgical Research, Oslo University Hospital, Rikshospitalet, Oslo, Norway
7Institute of Clinical Medicine, University of Oslo, Oslo, Norway
8Department of Cardiology, Oslo University Hospital, Rikshospitalet, Oslo, Norway
9Section of Clinical Immunology and Infectious Diseases, Oslo University Hospital, Rikshospitalet, Oslo, Norway
10Department of Internal Medicine, Diakonhjemmet Hospital, Oslo, Norway

Correspondence should be addressed to Yangchen Dhondup; moc.liamg@dehcgnay

Received 23 November 2016; Revised 24 February 2017; Accepted 7 March 2017; Published 11 April 2017

Academic Editor: Elzbieta Kolaczkowska

Copyright © 2017 Yangchen Dhondup et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Aim. Inflammation is important in heart failure (HF). The role of the immune receptor toll-like receptor 9 (TLR9) in HF is not understood and not investigated in diastolic HF. We investigated the role of TLR9 in a murine diastolic HF model caused by cardiomyocyte SERCA2a excision. Methods and Results. We crossed SERCA2a KO and TLR9 KO mice to generate four mouse lines. Tamoxifen-induced cardiomyocyte SERCA2a gene excision was carried out in mice, causing diastolic HF. After 7.6 weeks, cardiac functions and dimensions were analyzed by echocardiography and heart tissues were processed. HF mice depleted of TLR9 demonstrated reduced survival compared to SERC2a KO mice, with a median life expectancy of 58 days compared to 63 days. Both HF groups displayed increased left atrium size, lung weight, fetal gene expressions, monocyte/macrophage infiltration, and fibrosis. However, there were no significant differences between the groups. Conclusion. In mice with SERCA2a KO-induced diastolic HF, the absence of TLR9 reduced median life expectancy. The cause remains elusive, as all investigated HF parameters were unaltered. Still, these findings support a salutary role of TLR9 in some subsets of HF conditions and underline the importance for future studies on the mechanisms of TLR9 in diastolic HF.