Stem cell factor/c-kit signaling mediated cardiac stem cell migration via activation of p38 MAPK

Kuang, Dong; Zhao, Xia; Xiao, Guixiang; Ni, Juan; Feng, Yongzeng; Wu, Renliang; Wang, Guoping

doi:10.1007/s00395-007-0690-z

Cited by 81 publications

(79 citation statements)

References 40 publications

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“…In vitro experiments have suggested that SCF induces ckit þ CSC migration in a concentration dependent manner that could be antagonized by antibody against c-kit. Furthermore, the SCF-induced migration of c-kit þ CSCs to infarcted myocardium was blocked by the inhibition of p38-MARK in vivo (Kuang et al, 2008). These results suggest that the SCF/c-kit mediate migration of c-kit þ CSCs and that migration of stem cells induced by SCF/ckit and SDF-1/CXCR4 pathways may share downstream p38-MAPK signaling pathways.…”

Section: Stem Cell Factor/c-kitmentioning

confidence: 78%

“…Kuang et al (2008) have demonstrated that the expression of SCF is significantly increased in the region immediately adjacent to the infarct (the peri-infarct myocardium) following MI in rats. The authors of these studies found higher expression of SCF in peri-infarct regions associated with an accumulation of transplanted c-kit þ CSCs.…”

Section: Stem Cell Factor/c-kitmentioning

confidence: 99%

“…CSCs have been shown to be able to migrate to the site of injury within the heart and participate in repairing damaged myocardium, leading to improved cardiac function following MI in different experimental MI models (Beltrami et al, 2003;Messina et al, 2004;Oh et al, 2004;Linke et al, 2005). The migration of CSCs to the infarct site is regulated by several signaling factors and pathways that are not yet fully understood Kuang et al, 2008;Tang et al, 2009). In this review, we will briefly discuss the role of CSCs in cardiomyocyte homeostasis, myocardial repair and regeneration, and provide an overview of the signaling factors and pathways involved in CSC migration.…”

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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: Stem Cell Factor/c-kitmentioning

confidence: 78%

Section: Stem Cell Factor/c-kitmentioning

confidence: 99%

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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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“…Subsequently, the cells that adhere to the blood vessel endothelium, permeate the vessel walls to access the target tissue. With the help of SDF-1α, the secretion of more MMP-9, NO, and VEGF promote the mobilization of stem cells (Tang et al, 2007;Kuang et al, 2008;Gao et al, 2010;Huang et al, 2010;Takamiya et al, 2011). These paracrine factors, especially VEGF, are important for maintaining or improving normal vascular endothelial function.…”

Section: Discussionmentioning

confidence: 99%

Use of bone mesenchymal stem cells to treat rats with acute liver failure

Sf¹,

Jiang²,

Lh³

et al. 2014

Genet. Mol. Res.

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ABSTRACT. This study aimed to isolate mesenchymal stem cells from bone mesenchymal stem cells (BMSCs), determine their therapeutic potential for treating rats with acute liver failure (ALF), further explore the factors that induce liver failure mechanisms, and elucidate the role of bone marrow stem cell therapy and BMSCs on liver homing. We found that differentiation potential was present in BMSCs expressing high levels of CD29 and CD90. These cells improved liver functioning in vivo after transplantation into rat livers with D-galactosamine damage, as evidenced by the levels of alanine aminotransferase and aspartate aminotransferase returning to normal (low levels) in recipient ALF rats. A significant improvement in the liver functional test and histological findings was observed in the Stem cells and acute liver failure transplantation group after 120 and 168 h of transplantation (P < 0.05). Histological data revealed that hepatocyte cell apoptosis was lower in the transplantation group compared to the control groups (P < 0.05), and that the transplantation of BMSCs reduced liver inflammation, decreased hepatic denaturation and necrosis, and promoted liver regeneration. These ameliorations were not recorded in the control groups. The results of in situ hybridization, immunofluorescence staining, and Western blot confirmed the presence of transplanted BMSCs in recipient rat livers. Stromal cell derived factor-1 alpha and vascular endothelial growth factor were significantly upregulated after the intraportal transplantation of BMSCs, with significantly higher levels being found in the portal vein and the tail vein groups (P < 0.05). In conclusion, BMSCs have a therapeutic effect against ALF rats, evoke endogenous repair mechanisms in the liver, and may represent a novel form of therapeutic intervention for the disease. Furthermore, intraportal transplantation serves as a more effective pathway compared to tail vein transplantation.

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“…SCF/c-KIT effects mediating cell migration also depend on the MAPK pathway via phosphorylation and activity of p38 (Kuang et al 2008); MEK/MAPK inhibitors reduced the response to c-KIT by 30% (Farini et al 2007). …”

Section: The Mapk Pathwaymentioning

confidence: 99%