Increased inflammatory response and neovascularization in reperfused vs. nonreperfused murine myocardial infarction

Vandervelde, Susanne; Amerongen, Machteld J. van; Tio, René A.; Petersen, Arjen H.; Luyn, Marja J. A. van; Harmsen, Martin C.

doi:10.1016/j.carpath.2005.10.006

Cited by 85 publications

(78 citation statements)

References 9 publications

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“…To examine the possibility that inflammatory cells in the infarcted myocardium contribute to the GFP evaluation by uptake or cell fusion, we performed costaining studies of the myocardium 3 d post-MI for GFP and for neutrophils (anti-mouse neutrophil mAb MCA771GA; Serotec, Oxford, United Kingdom), macrophage (anti-mouse Mac-3 mAb), and toxic T lymphocytes (anti-mouse CD8 mAb). We found abundant neutrophils and macrophages (but a much lower amount of toxic T cells) in the infarct (Dewald et al, 2004;Vandervelde et al, 2006). None of the inflammatory cells were found GFP positive (data not shown), indicating that cell fusion or uptake of GFP by inflammatory cells, if existed, was extremely rare.…”

Section: Functional Validation Of Receptor/ligand Pairs With Antibodymentioning

confidence: 64%

Mesenchymal Stem Cells Use Integrin β1 Not CXC Chemokine Receptor 4 for Myocardial Migration and Engraftment

Huang

et al. 2007

MBoC

217

145

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Recent evidence has demonstrated the importance of bone marrow-derived mesenchymal stem cells (BM-MSCs) in the repair of damaged myocardium. The molecular mechanisms of engraftment and migration of BM-MSCs in the ischemic myocardium are unknown. In this study, we developed a functional genomics approach toward the identification of mediators of engraftment and migration of BM-MSCs within the ischemic myocardium. Our strategy involves microarray profiling (>22,000 probes) of ischemic hearts, complemented by reverse transcription-polymerase chain reaction and fluorescence-activated cell sorting of corresponding adhesion molecule and cytokine receptors in BM-MSCs to focus on the coexpressed pairs only. Our data revealed nine complementary adhesion molecules and cytokine receptors, including integrin ␤1, integrin ␣4, and CXC chemokine receptor 4 (CXCR4). To examine their functional contributions, we first blocked selectively these receptors by preincubation of BM-MSCs with specific neutralizing antibodies, and then we administered these cells intramyocardially. A significant reduction in the total number of BM-MSC in the infarcted myocardium was observed after integrin ␤1 blockade but not integrin ␣4 or CXCR4 blockade. The latter observation is distinctively different from that reported for hematopoietic stem cells (HSCs). Thus, our data show that BM-MSCs use a different pathway from HSCs for intramyocardial trafficking and engraftment. INTRODUCTIONCardiac repair and remodeling after ischemic injury involves myocyte hypertrophy, collagen deposition, and possibly ventricular dilatation (Sutton and Sharpe, 2000). Recent provocative data suggest that stem cells, either resident in the heart or originating from the bone marrow, may play an important role in the repair and regeneration of the injured myocardium (Anversa and Nadal-Ginard, 2002). We and others have shown that intramyocardial transplantation of bone marrow-derived stem cells (BMSCs) can promote cardiac repair with resulting functional improvement and reduced infarct size (Kocher et al., 2001;Mangi et al., 2003;Amado et al., 2005). In addition to direct transplantation, mobilization of BMSCs with cytokines such as granulocytecolony stimulating factor (G-CSF) and stem cell factor has been reported to enhance myocardial repair and improve cardiac function (Anversa and Nadal-Ginard, 2002;Askari et al., 2003). However, in a recent trial, the subcutaneous administration of G-CSF after acute myocardial infarction (MI) did not lead to further improvement in ventricular function compared with conventional treatment (Ripa et al., 2006). These controversial findings suggest the need to understand the molecular mechanisms involved with stem cell migration and engraftment into the infarcted myocardium.It has been reported that hematopoietic stem cells (HSCs) migrate in response to stromal-derived factor (SDF)-1␣, the ligand for the CXC chemokine receptor 4 (CXCR4) (Wright et al., 2002), and the up-regulation of SDF-1 in the ischemic myocardium mediates homing of HSCs vi...

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Section: Functional Validation Of Receptor/ligand Pairs With Antibodymentioning

confidence: 64%

Mesenchymal Stem Cells Use Integrin β1 Not CXC Chemokine Receptor 4 for Myocardial Migration and Engraftment

Huang

et al. 2007

MBoC

217

145

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show abstract

“…Prior histologic work in mice showed that the number of monocytes and/or macrophages in the infarct zone starts to increase 1-2 days after MI, reaches a maximum on day 4 after MI, and decreases thereafter from days 7-28 after MI (20,21). On the basis of these data, the timeline of our experiment was designed ( Fig E1 [online]) (all authors).…”

Section: Experimental Protocolmentioning

confidence: 99%

Monocyte and/or Macrophage Infiltration of Heart after Myocardial Infarction: MR Imaging by Using T1-shortening Liposomes

Naresh¹,

Xu²,

Klibanov³

et al. 2012

Radiology

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“…Several different features exist between the pathophysiology of permanent MI and I/R injury. 31, 32 Reperfusion releases a large excess of reactive oxygen species (ROS) and causes "reperfusion injury". Inflammatory responses such as infiltration by neutrophils and macrophages are much stronger in the reperfused heart than in the infarcted heart.…”

Section: Chemokines In MImentioning

confidence: 99%

Role of the SDF-1/CXCR4 System in Myocardial Infarction

Takahashi

2010

Circ J

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Increased inflammatory response and neovascularization in reperfused vs. nonreperfused murine myocardial infarction

Cited by 85 publications

References 9 publications

Mesenchymal Stem Cells Use Integrin β1 Not CXC Chemokine Receptor 4 for Myocardial Migration and Engraftment

Mesenchymal Stem Cells Use Integrin β1 Not CXC Chemokine Receptor 4 for Myocardial Migration and Engraftment

Monocyte and/or Macrophage Infiltration of Heart after Myocardial Infarction: MR Imaging by Using T1-shortening Liposomes

Role of the SDF-1/CXCR4 System in Myocardial Infarction

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