SCF increases cardiac stem cell migration through PI3K/AKT and MMP-2/-9 signaling

Guo, Junli; Jie, Wei; Shen, Zhihua; Li, Mengsen; Lan, You-Ling; Kong, Yue-Qiong; Guo, Shaoli; Li, Tianfa; Zheng, Shaojiang

doi:10.3892/ijmm.2014.1773

Cited by 39 publications

(33 citation statements)

References 39 publications

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“…The concentration of SCF needed to direct the migration of hMSCs was higher than previously reported. 26 This might be due to the methodology used to evaluate cell migration and/or the source of the SCF. The advantage of the current methodology is that chemotaxis slides allow observing the migration in linear and stable concentration profiles and distinguish between random migration from primed and directed migration.…”

Section: Discussionmentioning

confidence: 99%

Effects of Stem Cell Factor on Cell Homing During Functional Pulp Regeneration in Human Immature Teeth

Ruangsawasdi

Zehnder

Patcas

et al. 2017

Tissue Engineering Part A

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Conventional root canal treatment in immature permanent teeth can lead to early tooth loss in children because root formation is discontinued. We investigated whether the stem cell factor (SCF) could facilitate cell homing in the pulpless immature root canal and promote regeneration of a functional pulp. In vitro, human mesenchymal stem cells (hMSCs) were exposed to SCF at various concentrations for assessing cell migration, proliferation, and differentiation toward odonto/osteoblasts by 3D-chemotaxis slides, WST-1 assay, and alkaline phosphatase activity, respectively. Fibrin gels were used to deliver 15 g/mL SCF for in vivo experiments. The release kinetic of SCF was assessed in vitro. Two corresponding human immature premolars, with or without SCF, were placed at rat calvariae for 6 and 12 weeks. All tooth specimens were either analyzed histologically and the percentage of tissue ingrowth determined or the cells were extracted from the pulp space, and the mRNA level of DMP1, DSPP, Col1, NGF, and VEGF were assessed by quantitative polymerase chain reaction. In the presence of SCF, we saw an increase in hMSCs directional migration, proliferation, and odonto/osteogenic differentiation. SCF also increased the extent of tissue ingrowth at 6 weeks but not at 12 weeks. However, at this time point, the formed tissue appeared more mature in samples with SCF. In terms of gene transcription, DMP1, Col1, and VEGF were the significantly upregulated genes, while DSPP and NGF were not affected. Our results suggest that SCF can accelerate cell homing and the maturation of the pulp-dentin complex in human immature teeth. Conventional root canal treatment in immature permanent teeth can lead to early tooth loss in children because root formation is discontinued. We investigated whether the stem cell factor (SCF) could facilitate cell homing in the pulpless immature root canal and promote regeneration of a functional pulp. In vitro, human mesenchymal stem cells (hMSCs) were exposed to SCF at various concentrations for assessing cell migration, proliferation, and differentiation toward odonto/osteoblasts by 3D-chemotaxis slides, WST-1 assay, and alkaline phosphatase activity, respectively. Fibrin gels were used to deliver 15 mg/mL SCF for in vivo experiments. The release kinetic of SCF was assessed in vitro. Two corresponding human immature premolars, with or without SCF, were placed at rat calvariae for 6 and 12 weeks. All tooth specimens were either analyzed histologically and the percentage of tissue ingrowth determined or the cells were extracted from the pulp space, and the mRNA level of DMP1, DSPP, Col1, NGF, and VEGF were assessed by quantitative polymerase chain reaction. In the presence of SCF, we saw an increase in hMSCs directional migration, proliferation, and odonto/ osteogenic differentiation. SCF also increased the extent of tissue ingrowth at 6 weeks but not at 12 weeks. However, at this time point, the formed tissue appeared more mature in samples with SCF. In terms of gene transcription, DMP1, Col1, a...

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Section: Discussionmentioning

confidence: 99%

Effects of Stem Cell Factor on Cell Homing During Functional Pulp Regeneration in Human Immature Teeth

Ruangsawasdi

Zehnder

Patcas

et al. 2017

Tissue Engineering Part A

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“…It is also widely known that MSCs are capable of secreting various types of cytokines, including stem cell factor (SCF), thrombopoietin and interleukin-6 (11,12). These cytokines regulate stem cell differentiation, direct migration and mediate inflammatory processes (13–15). Therefore, cytokines secreted from MSCs may affect fracture coalescence.…”

Section: Introductionmentioning

confidence: 99%

HMGB1 promotes the secretion of multiple cytokines and potentiates the osteogenic differentiation of mesenchymal stem cells through the Ras/MAPK signaling pathway

Lin

Xue

Chen

et al. 2016

Experimental and Therapeutic Medicine

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High mobility group box 1 (HMGB1) protein has been previously been detected in the inflammatory microenvironment of bone fractures. It is well known that HMGB1 acts as a chemoattractant to mesenchymal stem cells (MSCs). In the present study, the effects of HMGB1 on cytokine secretion from MSCs were determined, and the molecular mechanisms underlying these effects of HMGB1 on osteogenic differentiation were elucidated. To detect cytokine secretion, antibody array assays were performed, which demonstrated that HGMB1 induced the differential secretion of cytokines that are predominantly associated with cell development, regulation of growth and cell migration, stress responses, and immune system functions. Moreover, the secretion of epidermal growth factor receptor (EGFR) was significantly upregulated by HMGB1. The EGFR-activated Ras/MAPK pathway regulates the osteogenic differentiation of MSCs. These results suggested that HMGB1 enhances the secretion of various cytokines by MSCs and promotes osteogenic differentiation via the Ras/MAPK signaling pathway. The present study may provide a theoretical basis for the development of novel techniques for the treatment of bone fractures in the future.

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“…SCF induces CPC migration in a concentration-dependent manner (126,177), and this process is inhibited by c-kit-blocking antibody (177). Gene transfer of SCF in vivo facilitates the functional recovery after myocardial infarction due to the expansion and mobilization of the pool of c-kit-positive CPCs (280,353).…”

Section: Cpc Mobilization In Response To Myocardial Injurymentioning

confidence: 99%

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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SCF increases cardiac stem cell migration through PI3K/AKT and MMP-2/-9 signaling

Cited by 39 publications

References 39 publications

Effects of Stem Cell Factor on Cell Homing During Functional Pulp Regeneration in Human Immature Teeth

Effects of Stem Cell Factor on Cell Homing During Functional Pulp Regeneration in Human Immature Teeth

HMGB1 promotes the secretion of multiple cytokines and potentiates the osteogenic differentiation of mesenchymal stem cells through the Ras/MAPK signaling pathway

Aging Effects on Cardiac Progenitor Cell Physiology

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