Differentiation and migration of Sca1+/CD31− cardiac side population cells in a murine myocardial ischemic model

Liang, Simon; Tan, T.; Gaudry, Leonie; Chong, Beng H.

doi:10.1016/j.ijcard.2008.08.032

Cited by 87 publications

(108 citation statements)

References 40 publications

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“…Studies have shown that the expression of SDF-1 was up-regulated in infarcted myocardium following MI (Pillarisetti and Gupta, 2001;Vandervelde et al, 2007). We have confirmed that SDF-1 upregulated in the infarcted myocardium, but moreover, its receptor, CXCR4 was upregulated on the SCA1 þ /CD31 -CSP cells (Liang et al, 2010). We hypothesized that the SDF-1/CXCR4 pathway might play an important role in the migration of CSP cells from noninfarcted area to the infarcted site within the myocardium where they subsequently differentiate into cells with a cardiomyocyte and endothelial like-phenotype.…”

Section: Sdf-1/cxcr4supporting

confidence: 77%

“…Pfister et al (2005) demonstrated that only SCA1 þ /CD31 À cardiac SP (CSP) cells were capable of differentiating into functional cardiomyocytes in vitro. We recently extended these findings, showing that following MI in mice SCA1 þ /CD31 À CSP cells migrated from nonischemic myocardium into the infarcted area where they differentiated into both cardiomyocyte-and endotheliallike cells (Liang et al, 2010). Our work further demonstrated that the second sub-population: SCA1 þ /CD31 þ CSP cells function as cardiac endothelial progenitor cells in mice.…”

Section: Resident Cscs Sca1 1 /Cd31 2 Cardiac Sp Cellssupporting

confidence: 72%

“…SP cells with stem cell-like properties in adult hearts were first reported by Hierlihy et al (2002). Since then, several groups, including ours, have confirmed the presence of such stem/progenitor cell populations in adult hearts (Martin et al, 2004;Pfister et al, 2005;Oyama et al, 2007;Liang et al, 2010).…”

Section: Resident Cscs Sca1 1 /Cd31 2 Cardiac Sp Cellssupporting

confidence: 62%

“…SCA1 þ /CD31 À and SCA1 þ /CD31 þ CSP both upregulated expression of C-X-C chemokine receptor type 4 (CXCR4) following MI. CXCR4 is a receptor for the chemotactic cytokine known as stromal-derived-factor-1 (SDF-1) (Liang et al, 2010;Liang et al, 2011). Similar findings were demonstrated in rats by Oyama et al (2007).…”

Section: Resident Cscs Sca1 1 /Cd31 2 Cardiac Sp Cellsmentioning

confidence: 59%

“…On the basis of the expression of stem cell antigen 1 (SCA1) and CD31, SP cells from the mouse heart can be divided into two subpopulations: SCA1 þ /CD31 À and SCA1 þ /CD31 þ (Pfister et al, 2005;Liang et al, 2010;Liang et al, 2011). Pfister et al (2005) demonstrated that only SCA1 þ /CD31 À cardiac SP (CSP) cells were capable of differentiating into functional cardiomyocytes in vitro.…”

Section: Resident Cscs Sca1 1 /Cd31 2 Cardiac Sp Cellsmentioning

confidence: 99%

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Migration of Resident Cardiac Stem Cells in Myocardial Infarction

Liang

Phillips

2012

The Anatomical Record

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Ischemic heart disease is a major cause of morbidity and mortality worldwide. Stem cell-based therapy, which aims to restore cardiac structure and function by regeneration of functional myocardium, has recently been proposed as a novel alternative treatment modality. Resident cardiac stem cells (CSCs) in adult hearts are a key cell type under investigation. CSCs have been shown to be able to repair damaged myocardium and improve myocardial function in both human and animal studies. This approach relies not only on the proliferation of the CSCs, but also upon their migration to the site of injury within the heart. Here, we briefly review reported CSC populations and discuss signaling factors and pathways required for the migration of CSCs. Anat Rec, 296:184-191, 2013. V C 2012 Wiley Periodicals, Inc.

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Section: Sdf-1/cxcr4supporting

confidence: 77%

Section: Resident Cscs Sca1 1 /Cd31 2 Cardiac Sp Cellssupporting

confidence: 72%

Section: Resident Cscs Sca1 1 /Cd31 2 Cardiac Sp Cellssupporting

confidence: 62%

Section: Resident Cscs Sca1 1 /Cd31 2 Cardiac Sp Cellsmentioning

confidence: 59%

Section: Resident Cscs Sca1 1 /Cd31 2 Cardiac Sp Cellsmentioning

confidence: 99%

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Migration of Resident Cardiac Stem Cells in Myocardial Infarction

Liang

Phillips

2012

The Anatomical Record

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Stem Cell Therapy of Myocardial Infarction: A Promising Opportunity in Bioengineering

Jiang

Shamul

et al. 2020

Advanced Therapeutics

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Myocardial infarction (MI) is a life‐threatening disease resulting from the irreversible death of cardiomyocytes (CMs). Stem cell‐based therapies have been studied for MI treatment over the last two decades with promising outcomes. Here, the past work in this field is critically reviewed to elucidate the advantages and disadvantages of treating MI using pluripotent stem cells (PSCs) including both embryonic stem cells (ESCs) and induced pluripotent stem cells (iPSCs), adult stem cells, and cardiac progenitor cells. Overall, PSCs (particularly iPSCs) have more advantages than the other cells for cardiac regeneration. However, the use of iPSCs is also facing critical challenges, which may be resolved by using biomaterials to engineer stem cells for reduced immunogenicity, improved immobilization/survival in the heart, and increased integration with the host cardiac tissue to eliminate arrhythmia. Biomaterials have also been applied in the derivation of CMs in vitro to increase the efficiency and maturation of cardiac differentiation. Collectively, a lot has been learned from the past failures of simply injecting intact stem cells or their derivatives in vivo for treating MI, and bioengineering stem cells with biomaterials may be a valuable strategy for advancing stem cell therapy towards its widespread application for MI treatment in the clinic.

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Knockdown of nucleosome assembly protein 1‐like 1 promotes dimethyl sulfoxide‐induced differentiation of P19CL6 cells into cardiomyocytes

Gong

et al. 2012

J of Cellular Biochemistry

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Transplantation of cardiomyocytes derived from stem cells is a promising option for cardiac repair. However, how to obtain efficient cardiomyocytes from stem cells is still a great challenge. Understanding of the mechanism that regulates the cardiac differentiation of stem cells is necessary for the effective induction of cardiomyocytes. A clonal derivative named P19CL6 cells can easily differentiate into cardiomyocytes with 1% dimethyl sulfoxide (DMSO) treatment, which offers a valuable model to study cardiomyocytes differentiation in vitro. In this study, the isobaric tags for relative and absolute quantitation (iTRAQ) proteomics were performed to identify proteins associated with cardiomyocytes differentiation of P19CL6 cells induced by DMSO. Out of 543 non-redundant proteins identified, 207 proteins showed significant changes during differentiation with ≥1.2-fold or ≤0.83-fold changes cut-offs. Nine proteins were confirmed by the quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot analysis respectively. Notably, broad consistency was well showed between mRNA and protein expression for down-regulation of nucleosome assembly protein 1-like 1 (Nap1l1). Further study revealed that knockdown of Nap1l1 by stable transfection of shRNA vector significantly accelerated DMSO-induced cardiomyocytes differentiation of P19CL6 cells characterized by increases in expression of cardiac specific transcription factors, genes, and proteins (GATA4, MEF-2C, ANP, BNP, cTNT, and β-MHC). Therefore, Nap1l1 is a novel protein that regulates cardiomyocytes differentiation of P19CL6 cells induced by DMSO.

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Differentiation and migration of Sca1+/CD31− cardiac side population cells in a murine myocardial ischemic model

Cited by 87 publications

References 40 publications

Migration of Resident Cardiac Stem Cells in Myocardial Infarction

Migration of Resident Cardiac Stem Cells in Myocardial Infarction

Stem Cell Therapy of Myocardial Infarction: A Promising Opportunity in Bioengineering

Knockdown of nucleosome assembly protein 1‐like 1 promotes dimethyl sulfoxide‐induced differentiation of P19CL6 cells into cardiomyocytes

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