Chronic myocardial infarction in the mouse: cardiac structural and functional change

Lutgens, Esther; Daemen, M. J. A. P.; Muinck, Ebo D. de; Debets, Jacques; Leenders, Peter; Smits, J. F. M.

doi:10.1016/s0008-6363(98)00216-8

Cited by 169 publications

(117 citation statements)

References 17 publications

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“…First, we demonstrated that cNGR-OG488 labeling was restricted to the BZ and IA at 4 and 7 days after MI with a local advantage of 2.3. Earlier histological observations in this model 10 that are supported by the current TPLSM data showed that the infarct and border zone were highly vascularized at this time. Second, as opposed to the plasma T 1/2 of the cNGR label, the tissue residence time of cNGR label was 9.1 hours, and this could be competed out with unlabeled cNGR, showing reversibility of binding and specificity of the cNGR moiety.…”

Section: Discussionsupporting

confidence: 83%

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cNGR: A Novel Homing Sequence for CD13/APN Targeted Molecular Imaging of Murine Cardiac Angiogenesis In Vivo

Buehler¹,

Zandvoort²,

Stelt³

et al. 2006

ATVB

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Objective-Previously, the peptide sequence cNGR has been shown to home specifically to CD13/APN (aminopeptidase N) on tumor endothelium. Here, we investigated the feasibility of selective imaging of cardiac angiogenesis using the cNGR-CD13/APN system. Methods and Results-CD13/APN induction and cNGR homing were studied in the murine myocardial infarction (MI) model. By real-time polymerase chain reaction (PCR) at 7 days after MI, CD13/APN expression was 10-to 20-fold higher in the angiogenic infarct border zone and the MI area than in non-MI areas. In vivo fluorescence microscopy confirmed specific homing of fluorophore-tagged cNGR to the border zone and MI territory at 4 and 7 days after MI with a local advantage of 2.3, but not at 1 or 14 days after MI. Tissue residence half-life was 9.1Ϯ0.3 hours, whereas the half-life in plasma was 15.4Ϯ3.4 minutes. Pulse chase experiments confirmed reversible binding of cNGR in the infarct area. Fluorescent labeled cNGR conjugates or antibodies were injected in vivo, and their distribution was studied ex vivo by 2-photon laser scanning microscopy (TPLSM). cNGR co-localized exclusively with CD13/APN and the endothelial marker CD31 on vessels. Conclusions-In cardiac angiogenesis endothelial CD13/APN is upregulated. It can be targeted specifically with cNGR conjugates. In the heart cNGR binds its endothelial target only in angiogenic areas.

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Section: Discussionsupporting

confidence: 83%

“…10 The wound healing response leads to angiogenesis in the border zone (BZ) and in the infarct area (IA). The IA could clearly be distinguished morphologically and the BZ was the area between the infarcted and the still viable myocardium.…”

Section: Murine Myocardial Infarctionmentioning

confidence: 99%

cNGR: A Novel Homing Sequence for CD13/APN Targeted Molecular Imaging of Murine Cardiac Angiogenesis In Vivo

Buehler¹,

Zandvoort²,

Stelt³

et al. 2006

ATVB

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“…Transverse sections of the heart, which were prepared as previously described, 17 were stained with hematoxylin and eosin or anti-desmin antibody and observed by light microscopy.…”

Section: Histopathological Examinationmentioning

confidence: 99%

Raloxifene Prevents Cardiac Hypertrophy and Dysfunction in Pressure-Overloaded Mice

Ogita

Node²,

Liao³

et al. 2004

Hypertension

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Abstract-17␤-Estradiol reduces myocardial hypertrophy and left ventricular mass, suggesting that the selective estrogen receptor modulator raloxifene may have similar effects. However, it is not clear whether raloxifene inhibits both cardiac hypertrophy and dysfunction. We used transverse aortic-banded mice to produce pressure-overload cardiac hypertrophy and used neonatal rat ventricular cardiomyocytes to investigate the cellular mechanisms of raloxifene on cardiac hypertrophy. Left ventricular mass and fractional shortening of mice hearts were measured by transthoracic echocardiography. Protein synthesis of cardiomyocytes was evaluated by incorporation of [ 3 H]leucine into cardiomyocytes exposed to angiotensin II. Phosphorylation of mitogen-activated protein (MAP) kinase was also observed in cardiomyocytes. Raloxifene prevented increases in left ventricular mass and decreases of fractional shortening at 4 weeks after aortic banding. Pretreatment with raloxifene before angiotensin II stimulation inhibited the increase in [3 H]leucine incorporation into neonatal rat cardiomyocytes in a concentration-dependent manner. This inhibition was partially but not significantly attenuated by N G -nitro-L-arginine methyl ester (L-NAME), an inhibitor of nitric oxide synthase, and completely abolished by ICI182780, an estrogen receptor antagonist. Although the phosphorylation of p38 MAP kinase, c-Jun N-terminal kinase (JNK), or extracellular signal-regulated protein kinase (ERK) in cardiomyocytes was significantly increased by angiotensin II stimulation as compared with the control, pretreatment with raloxifene attenuated p38 MAP kinase phosphorylation, but neither JNK nor ERK phosphorylation. We conclude that raloxifene inhibits cardiac hypertrophy and dysfunction and that the inhibition of p38 MAP kinase phosphorylation after the stimulation of estrogen receptors may be involved in the cellular mechanisms of this agent. Key Words: echocardiography Ⅲ heart failure Ⅲ hormones Ⅲ hypertrophy Ⅲ signal transduction T he incidence of left ventricular hypertrophy caused by essential hypertension is one of the major causes of impaired cardiac function followed by heart failure. 1,2 Although the increase in left ventricular mass may represent adaptation of the heart in response to pressure overload, left ventricular hypertrophy is associated with an increased risk of cardiovascular complications and mortality/morbidity. 2-5 Reduction or prevention of left ventricular hypertrophy by treatment with appropriate antihypertensive drugs reduces the risk of cardiovascular diseases or death. 6,7 In postmenopausal women, left ventricular hypertrophy is common and is likely to be a strong cardiovascular risk factor compared with men, suggesting that estrogen has potential protective effects in the cardiovascular system. 2 In fact, hormone replacement therapy in hypertensive postmenopausal women contributes to reducing left ventricular mass, improving cardiac function, and decreasing future cardiovascular events. 8 -10 However, the applicati...

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“…In two mice myocardial infarction was induced by ligating the left anterior descending (LAD) coronary artery four days before the examination, using published procedures [37].…”

Section: Mouse Preparationmentioning

confidence: 99%

Magnetic resonance imaging of regional cardiac function in the mouse

Heijman

Strijkers

Habets

et al. 2004

MAGMA

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In this paper we introduce an improved harmonic phase (HARP) analysis for complementary spatial modulation of magnetization (CSPAMM) tagging of the mouse left ventricular wall, which enables the determination of regional displacement fields with the same resolution as the corresponding CINE anatomical images. CINE MRI was used to measure global function, such as the ejection fraction. The method was tested on two healthy mouse hearts and two mouse hearts with a myocardial infarction, which was induced by a ligation of the left anterior descending coronary artery. We show that the regional displacement fields can be determined. The mean circumferential strain for the left ventricular wall of one of the healthy mice was −0.09 ± 0.04 (mean ± standard deviation), while for one of the infarcted mouse hearts strains of −0.02 ± 0.02 and −0.10 ± 0.03 were found in the infarcted and remote regions, respectively.

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Chronic myocardial infarction in the mouse: cardiac structural and functional change

Cited by 169 publications

References 17 publications

cNGR: A Novel Homing Sequence for CD13/APN Targeted Molecular Imaging of Murine Cardiac Angiogenesis In Vivo

cNGR: A Novel Homing Sequence for CD13/APN Targeted Molecular Imaging of Murine Cardiac Angiogenesis In Vivo

Raloxifene Prevents Cardiac Hypertrophy and Dysfunction in Pressure-Overloaded Mice

Magnetic resonance imaging of regional cardiac function in the mouse

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