Icariin Promotes the Migration of BMSCs In Vitro and In Vivo via the MAPK Signaling Pathway

Jiao, Feng; Tang, Wang; Huang, He; Zhang, Zhaofei; Liu, Donghua; Zhang, Hongyi; Ren, Hui

doi:10.1155/2018/2562105

Cited by 25 publications

(17 citation statements)

References 31 publications

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“…ICA also promotes CXCR4 expression, which is a signaling molecule upstream of MAPK, in BMSC migration through the activation of hypoxia inducible factor-1 (HIF-1) (Zhu et al, 2018). Moreover, transplantation of ICA-treated BMSCs in a cartilagedeficient rabbit model, accelerated the migration of BMSCs to the cartilage-deficient region in comparison to non-treated BMSCs (Jiao et al, 2018). These results suggest that ICA-treated BMSC may be effective in treating cartilage defects.…”

Section: Icariinmentioning

confidence: 83%

“…Astragalus membranaceus (Leguminosae) Li et al, 2017b Anti-oxidant, Anti-inflammatory, Cardio-protective, Neuro-protective, Hepato-protective, Nephro-protective, Anti-cancer Li et al, 2017b, Improvement of ventricular function in ischemic heart disease Xu et al, 2007 migration and bone differentiation, and is currently being therapeutically developed, for example in sustained-release drugs from the encapsulated microspheres of biodegradable polymers, it represents a potentially advanced option for bone repair (Schmuhl et al, 2014;Kamali et al, 2019). ICA, when used to pretreat MSCs, promote their migration to cartilage-defect sites (Jiao et al, 2018;Zhu et al, 2018), as well as their proliferation (Qin et al, 2015), bone differentiation (Li et al, 2015), and cartilage differentiation (Wang et al, 2014), and thus, may significantly improve healing related to skeletal defects. Tan IIA has been shown to increase CXCL12 expression at the site of injury as well as CXCR4 on transplanted MSCs, leading to enhanced MSC migration to the injured area, which may prove effective in the treatment of ischemic heart disease (Tong et al, 2011).…”

Section: Discussionmentioning

confidence: 99%

“…ICA administered at 1 µM was reported to significantly increase BMSC migration by stimulating actin stress fiber formation (Jiao et al, 2018). MAPK signals, such as p38, Erk1/2 and JNK, were activated during BMSC migration following ICA stimulation.…”

Section: Icariinmentioning

confidence: 92%

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Recruitment of Mesenchymal Stem Cells to Damaged Sites by Plant-Derived Components

Maeda

2020

Front. Cell Dev. Biol.

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Mesenchymal stem cells (MSCs) are capable of differentiating into a limited number of diverse cells and secrete regenerative factors that contribute to the repair of damaged tissue. In response to signals emitted by tissue damage, MSCs migrate from the bone marrow and area surrounding blood vessels within tissues into the circulating blood, and accumulate at the site of damage. Hence, MSC transplantation therapy is beginning to be applied to the treatment of various intractable human diseases. Recent medicinal plants studies have shown that plant-derived components can activate cell functions. For example, several plant-derived components activate cell signaling pathways, such as phosphatidylinositol 3-kinase and mitogen-activated protein kinase (MAPK), enhance expression of the CXCL12/CXCR4 axis, stimulate extracellular matrix remodeling, and consequently, promote cell migration of MSCs. Moreover, plant-derived components have been shown to promote recruitment of MSCs to damaged tissues and enhance healing in disease models, potentially advancing their therapeutic use. This article provides a comprehensive review of several plant-derived components that activate MSC migration and homing to damaged sites to promote tissue repair.

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Section: Icariinmentioning

confidence: 83%

Section: Discussionmentioning

confidence: 99%

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Recruitment of Mesenchymal Stem Cells to Damaged Sites by Plant-Derived Components

Maeda

2020

Front. Cell Dev. Biol.

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“…Interestingly, the relationship between cAMP signaling pathway and BMSCs has been documented [31]. In addition, Rap1 signaling pathway [32], regulation of actin cytoskeleton [33], signaling pathways regulating pluripotency of stem cells [34], focal adhesion [35], Hippo signaling pathway [36] and MAPK signaling pathway [37] that enriched in the current investigation have been reported to be closely related to stem cell biology. The results of GO and KEGG bioinformatics analysis suggest that the differentially methylated CpG islands and DMRs caused by SETD4 KO contain complex mechanisms that regulate BMSC biology.…”

Section: Discussionmentioning

confidence: 70%

SET domain-containing protein 4: biological functions and role in genomic methylation profiles of bone marrow mesenchymal stem cells

Liao

Shao

et al. 2020

Preprint

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Background: Epigenetic modification is a crucial mechanism affecting the biological function of stem cells. SETD4 is a histone methyltransferase, and its biological role in bone marrow mesenchymal stem cells (BMSCs) is currently unknown. This work was aimed to reveal the SETD4 biological role as well as its impacts on the genomic methylation profiles in BMSCs. Methods: BMSCs were isolated form SETD4 knockout (KO) and wild type (WT) mice that established by CRISPR/Cas9 technology. The cell proliferation, migration, myogenic differentiation and angiogenesis were tested according to appropriate biology techniques. And the Reduced Representation Bisulfite Sequencing (RRBS) method was adopted to analyze the global genomic methylation profiles of BMSCs, following bioinformatics analysis of GO functions and KEGG signaling of differential methylated CpG sites and differential methylation regions (DMRs). Finally, validation experiments were conducted to examine the expression of histone lysine methyltransferase and some representative genes. Results: SETD4 KO significantly promoted BMSCs proliferation, which was characterized by enhanced cell viability and increased expression of PCNA, Cyclin A2, Cyclin E1, CDK2, CDK6, Bcl2 and decreased the expression of P16, P21 and Caspase3. SETD4 deficiency impaired BMSCs migration and myogenic differentiation potentials, and even the angiogenesis via paracrine of VEGF. Compared with WT control, the overall genomic methylation of BMSCs in the SETD4 KO group only was decreased by 0.47%. However, the changed genomic methylation covers a total of 96,331 differential methylated CpG sites and 8692 DMR, with part of them settled in promoter regions. GO and KEGG analysis revealed that differential CpG islands and DMRs in promotes impacted 270 GO functions and 34 KEGG signaling pathways, with some closely related to stem cell biology. SETD4 KO inhibited sets of monomethylases and dimethylases for histone lysine, along with significant changes in some factors including Nkx2.5, Gata4, Gli2, Grem2, E2f7, Map7, Nr2f2 and Shox2 that associated with stem cell biology. Conclusions: These results are the first to reveal that even though SETD4 changes the genome’s overall methylation to a limited extent in BMSCs, it still affects the numerous cellular functions and signaling pathways, implying SETD4-altered genomic methylation serves a crucial molecular role in BMSCs’ biological functions.

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“…MAPK signaling pathways participate in the osteogenic differentiation and migration of hBMSCs. [22][23][24] The that they acted together on RUNX2 to induce osteogenic differentiation. 26 We found that the miR-23 mimic could inhibit the activity of p-p38, whereas it had no effect on p-JNK expression.…”

Section: Inhibition Of Mef2c Significantly Decreases Osteogenic Capmentioning

confidence: 99%

MicroRNA‐23 suppresses osteogenic differentiation of human bone marrow mesenchymal stem cells by targeting the MEF2C‐mediated MAPK signaling pathway

Jiang

Teng

Chen

2020

The Journal of Gene Medicine

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Background: The present study aimed to determine the role and mechanism of miR-23 with respect to regulating the osteogenic differentiation of human bone marrow mesenchymal stem cells (hBMSCs). Materials: The expression of miR-23 and MEF2C was measured in osteoporosis (OP) patients and healthy controls by a quantitative reverse transcriptase-polymerase chain reaction (qRT-PCR). The correlation between miR-23 and MEF2C was determined by the Pearson correlation coefficient. Moreover, bioinformatic analysis was performed using public databases. Target gene function and potential pathways were further examined. Then, we used a miR-23 mimic or inhibitor to further explore the potential mechanism of miR-23. Results: miR-23 is found to be up-regulated and MEF2C is down-regulated in OP patients compared to healthy controls. miR-23 had a negative correlation with MEF2C (r = −0.937, p = 0.001). Bioinformatic analysis revealed that a total of 664 overlapping target genes were found in the TargetScan (http://www.targetscan. org), miRDB (http://mirdb.org) and miRanda (http://www.microrna.org/microrna/home.do) databases. Moreover, Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis indicated that miR-23 may regulate the mitogan-activated protein kinase (MAPK) signaling pathway. miR-23 is down-regulated and MEF2C is significantly up-regulated in the osteogenic differentiation of hBMSCs. MEF2C was significantly up-regulated in the osteogenic differentiation of hBMSCs. Overexpression of miR-23 significantly down-regulated alkaline phosphatase (ALP) activity and calcium deposition, whereas the miR-23 inhibitor had the opposite effects. Moreover, overexpression of miR-23 significantly decreased osteoblastrelated markers (Runx2, Osx, ALP and OCN). Further experiments confirmed that MEF2C is a direct target of miR-23. Moreover, the miR-23 mimic enhanced the expression of p-p38 but had no effect on p-JNK. Conclusions: miR-23 decreases the osteogenic differentiation of hBMSCs through the MEF2C/MAPK signaling pathway.

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Icariin Promotes the Migration of BMSCs In Vitro and In Vivo via the MAPK Signaling Pathway

Cited by 25 publications

References 31 publications

Recruitment of Mesenchymal Stem Cells to Damaged Sites by Plant-Derived Components

Recruitment of Mesenchymal Stem Cells to Damaged Sites by Plant-Derived Components

SET domain-containing protein 4: biological functions and role in genomic methylation profiles of bone marrow mesenchymal stem cells

MicroRNA‐23 suppresses osteogenic differentiation of human bone marrow mesenchymal stem cells by targeting the MEF2C‐mediated MAPK signaling pathway

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