The Great Unknown
In: Diplomatic history, Volume 38, Issue 5, p. 1156-1158
ISSN: 1467-7709
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In: Diplomatic history, Volume 38, Issue 5, p. 1156-1158
ISSN: 1467-7709
In: The American journal of sociology, Volume 1, Issue 4, p. 500-501
ISSN: 1537-5390
In: Journal of political economy, Volume 4, Issue 1, p. 94-96
ISSN: 1537-534X
In: Journal of political economy, Volume 3, Issue 3, p. 366-367
ISSN: 1537-534X
In: Political science quarterly: a nonpartisan journal devoted to the study and analysis of government, politics and international affairs ; PSQ, Volume 9, Issue 2, p. 324-327
ISSN: 1538-165X
In: Proceedings of the Academy of Political Science in the City of New York, Volume 2, Issue 3, p. 141
In: Socio-economic planning sciences: the international journal of public sector decision-making, Volume 27, Issue 3, p. 209-217
ISSN: 0038-0121
In: Political science quarterly: a nonpartisan journal devoted to the study and analysis of government, politics and international affairs ; PSQ, Volume 4, Issue 2, p. 352
ISSN: 1538-165X
Endogenous anti-inflammatory annexin-A1 (ANX-A1) plays an important role in preserving left ventricular (LV) viability and function after ischaemic insults in vitro, but its long-term cardioprotective actions in vivo are largely unknown. We tested the hypothesis that ANX-A1-deficiency exaggerates inflammation, haematopoietic stem progenitor cell (HSPC) activity and LV remodelling in response to myocardial ischaemia in vivo. Adult ANX - A1 -/- mice subjected to coronary artery occlusion exhibited increased infarct size and LV macrophage content after 24-48 h reperfusion compared with wildtype (WT) counterparts. In addition, ANX - A1 -/- mice exhibited greater expansion of HSPCs and altered pattern of HSPC mobilisation 8 days post-myocardial infarction, with increased circulating neutrophils and platelets, consistent with increased cardiac inflammation as a result of increased myeloid invading injured myocardium in response to MI. Furthermore, ANX - A1 -/- mice exhibited significantly increased expression of LV pro-inflammatory and pro-fibrotic genes and collagen deposition after MI compared to WT counterparts. ANX-A1-deficiency increased cardiac necrosis, inflammation, hypertrophy and fibrosis following MI, accompanied by exaggerated HSPC activity and impaired macrophage phenotype. These findings suggest that endogenous ANX-A1 regulates mobilisation and differentiation of HSPCs. Limiting excessive monocyte/neutrophil production may limit LV damage in vivo. Our findings support further development of novel ANX-A1-based therapies to improve cardiac outcomes after MI. ; This work was supported in part by both the National Health and Medical Research Council (NHMRC) of Australia, including APP1045140 (to R.H.R., X.M.G., Y.H.Y.), APP1083138 & APP1106154 (to A.J.M.), and the Victorian Government's Operational Infrastructure Support Program. R.H.R. and X.J.D. are NHMRC Senior Research Fellows (APP1059960; APP1043026 respectively), A.J.M. is an NHMRC Career Development Fellow (APP1085752) and a NHF Future Leader Fellow (100440). A.A.S. and S.B.F. are supported by Australian Postgraduate Awards.
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