P. gingivalis lipopolysaccharide intensifies inflammation post-myocardial infarction through matrix metalloproteinase-9.
P. gingivalis lipopolysaccharide intensifies inflammation post-myocardial infarction through matrix metalloproteinase-9.
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DOI：
10.1016/j.yjmcc.2014.09.007
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发表时间：
2014-11
影响因子：
5
通讯作者：
Lindsey, Merry L.
中科院分区：
文献类型：
--
作者：
DeLeon-Pennell, Kristine Y.;Bras, Lisandra E. de Castro;Iyer, Rugmani Padmanabhan;Bratton, Dustin R.;Jin, Yu-Fang;Ripplinger, Crystal M.;Lindsey, Merry L.
关键词：
牙周病（PD）与心肌梗死（MI）后死亡率增加密切相关;然而，其潜在机制尚不清楚。基质金属蛋白酶（MMP）-9水平与MI后左心室（LV）功能障碍和重塑直接相关。MI后，MMP-9由白细胞产生并调节炎症。我们已经表明，暴露于牙龈卟啉单胞菌脂多糖（PgLPS），一种在PD患者中鉴定的免疫调节分子，增加小鼠的LV MMP-9水平，并导致心脏炎症和功能障碍。确定循环PgLPS是否通过MMP-9依赖性机制加重MI后LV炎症反应。我们将野生型C57 BL/6 J和MMP-9−/−小鼠暴露于PgLPS（ATCC 33277）28天，然后进行MI，并在MI后持续递送PgLPS长达7天。我们发现全身水平的PgLPS 1）增加血浆和梗死LV中的MMP-9水平，导致MI后壁厚度减少和LV破裂的发生率增加，和2）增加全身和局部巨噬细胞趋化性，导致MI后M1巨噬细胞浸润加速和LV功能降低。MMP-9的缺失通过减轻PgLPS诱导的炎症反应而发挥保护作用。总之，MMP-9缺失通过减弱巨噬细胞介导的炎症而对PgLPS暴露具有心脏保护作用。
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 Porphyromonas gingivalis lipopolysaccharide (PgLPS), an immunomodulatory molecule identified in PD patients, increases LV MMP-9 levels in mice and leads to cardiac inflammation and dysfunction. 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.
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影响因子：
6
作者：
Bekes, Erin M.;Schweighofer, Bernhard;Deryugina, Elena I.
通讯作者：
Deryugina, Elena I.
影响因子：
20.3
作者：
Duluc, Dorothee;Delneste, Yves;Jeannin, Pascale
通讯作者：
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多分析物分析揭示了基质金属蛋白酶-9和单核细胞趋化蛋白-1作为心脏衰老的血浆生物标志物。
DOI：
10.1161/circgenetics.111.959981
发表时间：
2011-08-01
期刊：
Circulation. Cardiovascular genetics
影响因子：
--
作者：
Chiao YA;Dai Q;Zhang J;Lin J;Lopez EF;Ahuja SS;Chou YM;Lindsey ML;Jin YF
通讯作者：
Jin YF
DOI：
10.1161/atvbaha.106.138743
发表时间：
2007-06-01
影响因子：
8.7
作者：
Pussinen, Pirkko J.;Tuomisto, Karolina;Salomaa, Veikko
通讯作者：
Salomaa, Veikko
影响因子：
3.7
作者：
Papantonopoulos, Georgios;Takahashi, Keiso;Loos, Bruno G.
通讯作者：
Loos, Bruno G.