scholarly journals Bone Marrow Mesenchymal Stem Cells Inhibit the Function of Dendritic Cells by Secreting Galectin-1

2017 ◽  
Vol 2017 ◽  
pp. 1-19 ◽  
Author(s):  
Yue Zhang ◽  
Xia-hui Ge ◽  
Xue-Jun Guo ◽  
Si-bin Guan ◽  
Xiao-ming Li ◽  
...  
Keyword(s):  
Stem Cells ◽  
Bone Marrow ◽  
T Cells ◽  
Mesenchymal Stem Cells ◽  
Dendritic Cells ◽  
Mapk Pathway ◽  
Mapk Signaling ◽  
Mitogen Activated Protein Kinase ◽  
Mouse Bone Marrow

This study aimed to investigate whether bone marrow-derived mesenchymal stem cells (BM-MSCs) can inhibit function of dendritic cells (DCs) by secreting Galectin-1 (Gal-1). BM-MSCs have been shown to inhibit the maturation and function of DCs, further inhibiting the activation and proliferation of T cells. However, the detailed mechanism remains unknown. In this current study, MSCs and DCs derived from mouse bone marrow were cocultured using Transwell culture plates under different in vitro conditions. The results showed that as the ratio of MSC to DC of the coculture system increased and the coculture time of the two cells prolonged, the concentrations of Gal-1, interleukin- (IL-) 10, and IL-12 in the supernatants were increased and the protein expression of Gal-1 on and within DCs was also enhanced. The phosphorylation of extracellular signal-regulated kinase (ERK) pathway in DCs was boosted, whereas p38 mitogen-activated protein kinase (MAPK) pathway phosphorylation was weakened. Meanwhile, the expression of costimulatory molecules on the surface of DCs was decreased, and the proliferative effect of DCs on allogeneic T cells was also decreased. Therefore, this present study indicated that Gal-1 secreted from MSCs upregulated expression of Gal-1 and stimulated formation of tolerance immunophenotype on DCs, where the underlying mechanism was the regulation of the MAPK signaling pathway in DCs, thereby inhibiting the function of DCs.

scholarly journals Mesenchymal stem cells maintain the stemness of colon cancer stem cells via interleukin-8/mitogen-activated protein kinase signaling pathway

2020 ◽  
Vol 245 (6) ◽  
pp. 562-575
Author(s):  
Xiaoying Ma ◽  
Jiajun Liu ◽  
Xiaotong Yang ◽  
Kai Fang ◽  
Peiyong Zheng ◽  
...  
Keyword(s):  
Stem Cells ◽  
Bone Marrow ◽  
Colon Cancer ◽  
Mesenchymal Stem Cells ◽  
Signaling Pathway ◽  
Theoretical Basis ◽  
Mapk Signaling ◽  
Mitogen Activated Protein Kinase ◽  
Mitogen Activated Protein

Mesenchymal stem cells (MSCs) can act as a carrier in tumor therapy, and tumor suppressor gene-modified MSCs can reach and suppress the tumor. However, in the colon cancer microenvironment, MSCs could promote tumor growth and create the environment that is conducive to the survival of cancer stem cells (CSCs). This study discovered MSCs from three sources (bone marrow, adipose, placenta) could induce the stemness and epithelial–mesenchymal transition (EMT) of HCT116 in vitro, meanwhile adipose- and placenta-derived MSCs increase the proportion of CD133+/CD44+ HCT116. Then, we explored the interaction mechanism between CD133+/CD44+ HCT116 and MSCs by the bioinformatics and in vitro assays. After CD133+/CD44+ HCT116 were co-cultured with MSCs, many cytokines in MSCs were stimulated, including interleukin-8 (IL-8). The binding of IL-8/CXCR2 activates the downstream mitogen-activated protein kinase (MAPK) signaling pathway in colon CSCs, thereby promoting the stemness and EMT. However, inhibition of IL-8/CXCR2/Erk1/2 could reverse the effect of MSCs on CSC stemness. In addition, MSCs co-cultured with CD133+/CD44+ HCT116 produce a carcinoma-associated fibroblast phenotype via intracellular FGF10–PKA–Akt–β-catenin signaling, which can be attenuated by IL-8 peptide inhibitor. To conclude, IL-8 promotes the interaction between colon CSCs and MSCs, and activates the MAPK signaling pathway in colon CSCs, which provides a theoretical basis for the application of MSCs in clinical practice. Impact statement MSCs have the property of chemotaxis and they can migrate to the tumor site by paracrine pathway in the tumor environment, and then interact with tumor cells. Although a mass of studies have been conducted about the impact of MSCs on tumors, it is still controversial whether the exogenous MSCs promote or inhibit tumor growth. In this work, we evaluated the effects of MSCs from three sources (bone marrow, adipose, placenta) on the proliferation, stemness, and metastasis of the colon cancer cells both in vitro and in vivo. Then, we proved the IL-8/CXCR2/MAPK and FGF10–PKA–Akt–β-catenin signaling pathway which mediate the interplay between MSC and CD133+/CD44+ colon cancer cell. This research aims to provide a theoretical basis for the safe application of MSCs in the clinical treatment of colon cancer.

Differentiation of Mouse Bone-Marrow Mesenchymal Stem Cells into Motor Neuron Cells in vitro

2016 ◽  
Vol 19 (2) ◽  
pp. 111-116
Author(s):  
Rafal Hussamildeen Abdullah ◽  
◽  
Shahlla Mahdi Salih ◽  
Nahi Yosef Yaseen ◽  
Ahmed Majeed Al-Shammari ◽  
...  
Keyword(s):  
Stem Cells ◽  
Bone Marrow ◽  
Mesenchymal Stem Cells ◽  
Motor Neuron ◽  
Mouse Bone Marrow ◽  
Marrow Mesenchymal Stem Cells

scholarly journals Immune Suppressive Effects of Tonsil-Derived Mesenchymal Stem Cells on Mouse Bone-Marrow-Derived Dendritic Cells

2015 ◽  
Vol 2015 ◽  
pp. 1-12 ◽  
Author(s):  
Minhwa Park ◽  
Yu-Hee Kim ◽  
Jung-Hwa Ryu ◽  
So-Youn Woo ◽  
Kyung-Ha Ryu
Keyword(s):  
Stem Cells ◽  
Bone Marrow ◽  
Mesenchymal Stem Cells ◽  
Dendritic Cells ◽  
T Cell ◽  
Cell Therapy ◽  
T Cell Subsets ◽  
Regulatory Function ◽  
Mouse Bone Marrow ◽  
And Function

Mesenchymal stem cells (MSCs) are considered valuable sources for cell therapy because of their immune regulatory function. Here, we investigated the effects of tonsil-derived MSCs (T-MSCs) on the differentiation, maturation, and function of dendritic cells (DCs). We examined the effect of T-MSCs on differentiation and maturation of bone-marrow- (BM-) derived monocytes into DCs and we found suppressive effect of T-MSCs on DCs via direct contact as well as soluble mediators. Moreover, T cell proliferation, normally increased in the presence of DCs, was inhibited by T-MSCs. Differentiation of CD4+T cell subsets by the DC-T cell interaction also was inhibited by T-MSCs. The soluble mediators suppressed by T-MSCs were granulocyte-macrophage colony-stimulating factor (GM-CSF), RANTES, interleukin-6 (IL-6), and monocyte chemoattractant protein-1 (MCP-1). Taken together, T-MSCs exert immune modulatory function via suppression of the differentiation, maturation, and function of BM-derived DCs. Our data suggests that T-MSCs could be used as a novel source of stem cell therapy as immune modulators.

Effects of Donor Age, Gender, and In Vitro Cellular Aging on the Phenotypic, Functional, and Molecular Characteristics of Mouse Bone Marrow-Derived Mesenchymal Stem Cells

2011 ◽  
Vol 20 (9) ◽  
pp. 1549-1561 ◽  
Author(s):  
Olga Katsara ◽  
Louisa G. Mahaira ◽  
Eleni G. Iliopoulou ◽  
Ardiana Moustaki ◽  
Aristidis Antsaklis ◽  
...  
Keyword(s):  
Stem Cells ◽  
Bone Marrow ◽  
Mesenchymal Stem Cells ◽  
Cellular Aging ◽  
Molecular Characteristics ◽  
Mouse Bone Marrow ◽  
Donor Age

CKIP-1 contributes to osteogenic differentiation of mouse bone marrow mesenchymal stem cells

2021 ◽  
Vol 16 (9) ◽  
pp. 847-859
Author(s):  
Qiannan Niu ◽  
Shuning Shen ◽  
Jiaojiao He ◽  
Lei Wang
Keyword(s):  
Stem Cells ◽  
Bone Marrow ◽  
Mesenchymal Stem Cells ◽  
Mouse Model ◽  
Signaling Pathway ◽  
Mapk Signaling ◽  
Mapk Signaling Pathway ◽  
Negative Regulator ◽  
Mouse Bone Marrow ◽  
Marrow Mesenchymal Stem Cells

Background: Osteogenesis greatly depends on the differentiation of bone marrow mesenchymal stem cells (BMSCs). CKIP-1 is considered to be a negative regulator of BMSCs. Methods: We established a  CKIP-1 knockout mouse model, then isolated and cultured BMSCs from wild-type and knockout groups. Results: Our data demonstrated that CKIP-1 knockout significantly increased bone structure in the experimental mouse model and enhanced BMSC proliferation. CKIP-1 knockout contributed to osteoblastic and adipogenic differentiation. Furthermore, CKIP-1 regulated osteogenesis in BMSCs via the MAPK signaling pathway, and BMSCs from the  CKIP-1 knockout mice were effective in repairing the skull defect null mice. Conclusion: Our results concluded that silencing of CKIP-1 promoted osteogenesis in experimental mice and increased BMSCs differentiation via upregulation of the MAPK signaling pathway.

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