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  • Degousee, Norbert  (2)
  • Wang, Xing-Hua  (2)
  • 1
    Online Resource
    Online Resource
    Abstract 4301: Chimeric Mice Lacking Microsomal Prostaglandin E 2 Synthase-1 (mPGES) In Bone Marrow Develop Adverse Left Ventricular Remodelling After Myocardial Infarction
    Ovid Technologies (Wolters Kluwer Health) ; 2008
    In:  Circulation Vol. 118, No. suppl_18 ( 2008-10-28)
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 118, No. suppl_18 ( 2008-10-28)
    Abstract: Introduction. mPGES functions downstream from COX-2 in the inducible PGE 2 biosynthetic pathway, and can be expressed by cardiac myocytes and inflammatory cells. mPGES gene targeted mice (mPGES −/− ) develop LV dilation and impaired contractile function after MI. The purpose of this study was to determine if mPGES in bone marrow (BM) derived inflammatory cells regulates LV remodelling after MI. Methods. Six week old female mPGES +/+ mice were irradiated with 9.5 Gy and transplanted with BM from male mPGES +/+ or mPGES −/− mice (BM +/+ or BM −/− chimeras, respectively). After 10 weeks, the left coronary artery was ligated. Echocardiography was used to assess LV dimensions and function in vivo . After fixation in situ , LV dimensions and infarct volume was assessed by planimetry. The efficiency of BM transplantation, determined by the ratio of syr to gapdh DNA, measured by real time PCR, was 98%. Results. There was no difference in LV dimensions or function between BM +/+ and BM −/− mice before MI (not shown). Between 7 and 28 days post MI, ejection fraction did not change in BM +/+ mice, but decreased significantly in BM −/− mice (Table ). BM −/− mice also had a higher LV diameter (2.7 ± 0.1 vs. 3.1 ± 0.1 mm, p = 0.0001) and LV volume (14 ± 0.8 vs. 18 ± 1.0 mm 3 , p = 0.025) than BM +/+ mice 28 days after MI. In contrast, there was no difference in the percentage of infarcted LV, heart rate or cardiac output between BM +/+ and BM −/− mice after MI. Survival of BM +/+ vs. BM −/− 28 days after MI was similar (75% vs. 72%, log rank, p = 0.86). Conclusion. mPGES1 in bone marrow cells that localize to the heart after MI is necessary to maintain post infarction LV contractile function, and to prevent adverse LV remodelling. Use of mPGES inhibitors as substitutes for COX-2 inhibitors may be detrimental in patients with coronary artery disease.
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/circ.118.suppl_18.S_862-c
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2008
    detail.hit.zdb_id: 1466401-X
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  • 2
    Online Resource
    Online Resource
    Lack of Microsomal Prostaglandin E 2 Synthase-1 in Bone Marrow–Derived Myeloid Cells Impairs Left Ventricular Function and Increases Mortality After Acute Myocardial Infarction
    Ovid Technologies (Wolters Kluwer Health) ; 2012
    In:  Circulation Vol. 125, No. 23 ( 2012-06-12), p. 2904-2913
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 125, No. 23 ( 2012-06-12), p. 2904-2913
    Abstract: Microsomal prostaglandin E 2 synthase-1 (mPGES-1), encoded by the Ptges gene, catalyzes prostaglandin E 2 biosynthesis and is expressed by leukocytes, cardiac myocytes, and cardiac fibroblasts. Ptges −/− mice develop more left ventricle (LV) dilation, worse LV contractile function, and higher LV end-diastolic pressure than Ptges +/+ mice after myocardial infarction. In this study, we define the role of mPGES-1 in bone marrow–derived leukocytes in the recovery of LV function after coronary ligation. Methods and Results— Cardiac structure and function in Ptges +/+ mice with Ptges +/+ bone marrow ( BM +/+ ) and Ptges +/+ mice with Ptges −/− BM ( BM −/− ) were assessed by morphometric analysis, echocardiography, and invasive hemodynamics before and 7 and 28 days after myocardial infarction. Prostaglandin levels and prostaglandin biosynthetic enzyme gene expression were measured by liquid chromatography–tandem mass spectrometry and real-time polymerase chain reaction, immunoblotting, immunohistochemistry, and immunofluorescence microscopy, respectively. After myocardial infarction, BM −/− mice had more LV dilation, worse LV systolic and diastolic function, higher LV end-diastolic pressure, more cardiomyocyte hypertrophy, and higher mortality but similar infarct size and pulmonary edema compared with BM +/+ mice. BM −/− mice also had higher levels of COX-1 protein and more leukocytes in the infarct, but not the viable LV, than BM +/+ mice. Levels of prostaglandin E 2 were higher in the infarct and viable myocardium of BM −/− mice than in BM +/+ mice. Conclusions— Lack of mPGES-1 in bone marrow–derived leukocytes negatively regulates COX-1 expression, prostaglandin E 2 biosynthesis, and inflammation in the infarct and leads to impaired LV function, adverse LV remodeling, and decreased survival after acute myocardial infarction.
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/CIRCULATIONAHA.112.099754
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2012
    detail.hit.zdb_id: 1466401-X
    Location Call Number Limitation Availability
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