Journal
JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY
Volume 76, Issue -, Pages 218-226Publisher
ELSEVIER SCI LTD
DOI: 10.1016/j.yjmcc.2014.09.007
Keywords
Matrix metalloproteinase-9; Myocardial infarction; Periodontal disease; Porphyromonas gingivalis; Proteomics; Cardiac function
Categories
Funding
- American Heart Association [13POST14350034, 14SDG18860050, 14POST18770012]
- National Institute of Health/National Heart, Lung, and Blood Institute [R01 HL111600]
- HHSN [268201000036C (N01-HV-00244), R01HL075360]
- Biomedical Laboratory Research and Development Service of the Veterans Affairs Office of Research and Development Award [5I01BX000505]
- [HL051971]
- [GM104357]
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Periodontal disease (PD) strongly correlates with increased mortality post-myocardial infarction (MI); however, the underlying mechanisms are unknown. Matrix metalloproteinase (MMP)-9 levels directly correlate with dysfunction and remodeling of the left ventricle (LV) post-MI. Post-MI, MMP-9 is produced by leukocytes and modulates inflammation. We have shown that exposure to Pmphyromonas gingivalis lipopolysaccharide (PgLPS), an immunomodulatory molecule identified in PD patients, increases LV MMP-9 levels in mice and leads to cardiac inflammation and dysfunction. The aim of the study was to determine if circulating PgLPS exacerbates the LV inflammatory response post-MI through MMP-9 dependent mechanisms. We exposed wild type C57BL/6J and MMP-9(-/-) mice to PgLPS (ATCC 33277) for a period of 28 days before performing MI, and continued to deliver PgLPS for up to 7 days post-MI. We found systemic levels of PgLPS 1) increased MMP-9 levels in both plasma and infarcted LV resulting in reduced wall thickness and increased incidence of LV rupture post-MI and 2) increased systemic and local macrophage chemotaxis leading to accelerated M1 macrophage infiltration post-MI and decreased LV function. MMP-9 deletion played a protective role by attenuating the inflammation induced by systemic delivery of PgLPS. In conclusion, MMP-9 deletion has a cardioprotective role against PgLPS exposure, by attenuating macrophage mediated inflammation. (C) 2014 Elsevier Ltd. All rights reserved.
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