Migration of Resident Cardiac Stem Cells in Myocardial Infarction

Liang, Simon; Phillips, William D.

doi:10.1002/ar.22633

Cited by 18 publications

(20 citation statements)

References 82 publications

(126 reference statements)

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“…Experimental evidence indicates that CPCs are recruited to the site of myocardial injury and participate in the reparative process (117,120,203,273,330,340). Although the mechanisms that govern CPC migration are not fully understood, several factors affect the mobilization of resident progenitors to the area of tissue damage.…”

Section: Cpc Mobilization In Response To Myocardial Injurymentioning

confidence: 98%

Aging Effects on Cardiac Progenitor Cell Physiology

Rota

Goichberg

Anversa

et al. 2015

Comprehensive Physiology

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Cardiac aging has been confounded by the concept that the heart is a postmitotic organ characterized by a predetermined number of myocytes, which is established at birth and largely preserved throughout life until death of the organ and organism. Based on this premise, the age of cardiac cells should coincide with that of the organism; at any given time, the heart would be composed of a homogeneous population of myocytes of identical age. The discovery that stem cells reside in the heart and generate cardiac cell lineages has imposed a reconsideration of the mechanisms implicated in the manifestations of the aging myopathy. The progressive alterations of terminally differentiated myocytes, and vascular smooth muscle cells and endothelial cells may represent an epiphenomenon dictated by aging effects on cardiac progenitor cells (CPCs). Changes in the properties of CPCs with time may involve loss of self-renewing capacity, increased symmetric division with formation of daughter committed cells, partial depletion of the primitive pool, biased differentiation to the fibroblast fate, impaired ability to migrate, and forced entry into an irreversible quiescent state. Telomere shortening is a major variable of cellular senescence and organ aging, and support the notion that CPCs with critically shortened or dysfunctional telomeres contribute to myocardial aging and chronic heart failure. These defects constitute the critical variables that define the aging myopathy in humans. Importantly, a compartment of functionally competent human CPCs persists in the decompensated heart pointing to stem cell therapy as a novel form of treatment for the aging myopathy.

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Section: Cpc Mobilization In Response To Myocardial Injurymentioning

confidence: 98%

Aging Effects on Cardiac Progenitor Cell Physiology

Rota

Goichberg

Anversa

et al. 2015

Comprehensive Physiology

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“…translatable systems, ligand immobilization strategies have been attempted for controlled induction of Notch signaling [20]. Endogenous progenitor cells and other resident cells are known to migrate to the infarct site due to the signals present in the infarct and in response to the presence of SAP [21][22][23]. Moreover, following an infarction, an increase in levels of Notch activation along with increases in downstream targets and corresponding ligand expression has been observed [24].…”

Section: Introductionmentioning

confidence: 99%

Intramyocardial Delivery ofNotchLigand-Containing Hydrogels Improves Cardiac Function and Angiogenesis Following Infarction

Boopathy

Martinez

Smith

et al. 2015

Tissue Engineering Part A

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Myocardial infarction (MI) is the leading cause of death worldwide. Notch1 signaling plays a critical role in cardiac development, in survival, cardiogenic lineage commitment, differentiation of cardiac stem/progenitor cells, and in regenerative responses following myocardial injury. The objective of this study was the evaluation of the therapeutic effect of delivering the Notch ligand-containing hydrogels in a rat model of MI. Self-assembling peptide (SAP) hydrogels were functionalized with a peptide mimic of the Notch1 ligand Jagged1 (RJ). In rats subjected to experimental MI, delivery of RJ-containing hydrogel to the infarcted heart resulted in improvement in cardiac function back to sham-operated levels. A significant decrease in fibrosis and an increase in the endothelial vessel area and Ki67 expression were also observed in rats treated with the RJ hydrogels compared to untreated rats or rats treated with unmodified or scrambled peptide hydrogels. This study demonstrates the functional benefit of Notch1-activating peptide delivered in SAP hydrogels for cardiac repair.

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“…Besides, CSCs are able to migrate into the site of heart injury and participate in restoring myocardium that was damaged. So the cardioprotective effect of CSCs relies not only on its proliferation, but also on its ability to migrate towards injury within the heart [3]. Signaling factors and pathways that were shown to participate in CSCs migration process include hypoxia-inducible factor-1 α (HIF-1 α ), stromal cell-derived factor-1 (SDF-1)/CXCR4, stem cell factor (SCF)/c-kit, hepatocyte growth factor (HGF)/c-met, insulin-like growth factor-1 (IGF-1)/IGF-1R, erythropoietin (EPO)/EPOR, EphrinA1/EphA1 Receptor, and so on [4–6].…”

Section: Introductionmentioning

confidence: 99%

Matrix Metalloproteinase 9 Secreted by Hypoxia Cardiac Fibroblasts Triggers Cardiac Stem Cell Migration In Vitro

Gao

Guo

Zeng

et al. 2015

Stem Cells International

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Cessation of blood supply due to myocardial infarction (MI) leads to complicated pathological alteration in the affected regions. Cardiac stem cells (CSCs) migration plays a major role in promoting recovery of cardiac function and protecting cardiomyocytes in post-MI remodeling. Despite being the most abundant cell type in the mammalian heart, cardiac fibroblasts (CFs) were underestimated in the mechanism of CSCs migration. Our objective in this study is therefore to investigate the migration related factors secreted by hypoxia CFs in vitro and the degree that they contribute to CSCs migration. We found that supernatant from hypoxia induced CFs could accelerate CSCs migration. Four migration-related cytokines were reported upregulated both in mRNA and protein levels. Upon adding antagonists of these cytokines, the number of migration cells significantly declined. When the cocktail antagonists of all above four cytokines were added, the migration cells number reduced to the minimum level. Besides, MMP-9 had an important effect on triggering CSCs migration. As shown in our results, MMP-9 induced CSCs migration and the underlying mechanism might involve TNF-α signaling which induced VEGF and MMP-9 expression.

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Migration of Resident Cardiac Stem Cells in Myocardial Infarction

Cited by 18 publications

References 82 publications

Aging Effects on Cardiac Progenitor Cell Physiology

Aging Effects on Cardiac Progenitor Cell Physiology

Intramyocardial Delivery ofNotchLigand-Containing Hydrogels Improves Cardiac Function and Angiogenesis Following Infarction

Matrix Metalloproteinase 9 Secreted by Hypoxia Cardiac Fibroblasts Triggers Cardiac Stem Cell Migration In Vitro

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