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1.
BMB Rep ; 50(6): 341, 2017 Jun.
Article in English | MEDLINE | ID: mdl-28651685

ABSTRACT

The BMB Reports would like to correct in the ACKNOWLEDGEMENTS of BMB Rep. 45(12), 713-718 titled "Ganglioside GM1 influences the proliferation rate of mouse induced pluripotent stem cells".

2.
BMB Rep ; 46(11): 527-32, 2013 Nov.
Article in English | MEDLINE | ID: mdl-24152915

ABSTRACT

Gangliosides are complex glycosphingolipids that are the major component of cytoplasmic cell membranes, and play a role in the control of biological processes. Human mesenchymal stem cells (hMSCs) have received considerable attention as alternative sources of adult stem cells because of their potential to differentiate into multiple cell lineages. In this study, we focus on various functional roles of gangliosides in the differentiation of hMSCs into osteoblasts or neuronal cells. A relationship between gangliosides and epidermal growth factor receptor (EGFR) activation during osteoblastic differentiation of hMSCs was observed, and the gangliosides may play a major role in the regulation of the differentiation. The roles of gangliosides in osteoblast differentiation are dependent on the origin of hMSCs. The reduction of ganglioside biosynthesis inhibited the neuronal differentiation of hMSCs during an early stage of the differentiation process, and the ganglioside expression can be used as a marker for the identification of neuronal differentiation from hMSCs.


Subject(s)
Cell Differentiation , Gangliosides/metabolism , Mesenchymal Stem Cells/cytology , Neurogenesis , Osteoblasts/cytology , Osteogenesis , Adult Stem Cells/cytology , Cell Differentiation/drug effects , Cell Lineage , Gangliosides/pharmacology , Humans , Neurogenesis/drug effects , Neurons/cytology , Neurons/drug effects , Osteogenesis/drug effects
3.
Biotechnol Lett ; 35(12): 2031-8, 2013 Dec.
Article in English | MEDLINE | ID: mdl-24078119

ABSTRACT

An epithelial cell adhesion molecule (EpCAM) was selectively expressed in human colorectal carcinoma. Treatment with plant-derived anti-EpCAM mAb (mAbP CO17-1A) and RAW264.7 cells inhibited cell growth in the human colorectal cancer cell line SW620. In SW620 treated with mAbP CO17-1A and RAW264.7 cells, expression of p53 and p21 increased, whereas the expression of G1 phase-related proteins, cyclin D1, CDK4, cyclin E, and CDK2, decreased, similar to mammalian-derived mAb (mAbM) CO17-1A. Similar to mAbM CO17-1A, treatment with mAbP CO17-1A and RAW264.7 cell decreased the expression of anti-apoptotic protein, Bcl-2, but the expression of pro-apoptotic proteins Bax, TNF-α, caspase-3, caspase-6, caspase-8 and caspase-9, increased. Cells treated with mAbP CO17-1A and RAW264.7 cells expressed metastasis-related gangliosides, GM1 and GD1a, similar to mAbM CO17-1A. These results suggest that mAbP CO17-1A is as effective on anti-cancer activity as mAbM CO17-1A.


Subject(s)
Antibodies, Monoclonal/pharmacology , Antineoplastic Agents/pharmacology , Colonic Neoplasms/metabolism , Gangliosides/metabolism , Gene Expression Regulation, Neoplastic/drug effects , Plant Proteins/pharmacology , Apoptosis/drug effects , Cell Line, Tumor , Cell Survival/drug effects , Humans , Plants, Genetically Modified/metabolism , Recombinant Proteins/pharmacology
4.
BMB Rep ; 45(12): 713-8, 2012 Dec.
Article in English | MEDLINE | ID: mdl-23261057

ABSTRACT

Gangliosides play important roles in the control of several biological processes, including proliferation and transmembrane signaling. In this study, we demonstrate the effect of ganglioside GM1 on the proliferation of mouse induced pluripotent stem cells (miPSCs). The proliferation rate of miPSCs was lower than in mouse embryonic stem cells (mESCs). Fluorescence activated cell sorting analysis showed that the percentage of cells in the G2/M phase in miPSCs was lower than that in mESCs. GM1 was expressed in mESCs, but not miPSCs. To confirm the role of GM1 in miPSC proliferation, miPSCs were treated with GM1. GM1-treated miPSCs exhibited increased cell proliferation and a larger number of cells in the G2/M phase. Furthermore, phosphorylation of mitogen-activated protein kinases was increased in GM1- treated miPSCs.


Subject(s)
Cell Proliferation/drug effects , G(M1) Ganglioside/pharmacology , Induced Pluripotent Stem Cells/cytology , Animals , Cells, Cultured , Embryonic Stem Cells/cytology , Embryonic Stem Cells/metabolism , Flow Cytometry , G2 Phase Cell Cycle Checkpoints/drug effects , Induced Pluripotent Stem Cells/metabolism , M Phase Cell Cycle Checkpoints/drug effects , MAP Kinase Signaling System , Mice
5.
Lab Anim Res ; 28(4): 255-63, 2012 Dec.
Article in English | MEDLINE | ID: mdl-23326286

ABSTRACT

Gangliosides are ubiquitous components of the membranes of mammalian cells that are thought to play important roles in various cell functions such as cell-cell interaction, cell adhesion, cell differentiation, growth control, and signaling. However, the role that gangliosides play in the immune rejection response after xenotransplantation is not yet clearly understood. In this study, the regulatory effects of human leukocytes on ganglioside expression in primary cultured micro-pig aortic endothelial cells (PAECs) were investigated. To determine the impact of human leukocytes on the expression of gangliosides in PAECs, we performed high-performance thin layer chromatography (HPTLC) in PAECs incubated with FBS, FBS containing human leukocytes, human serum containing human leukocytes, and FBS containing TNF-α. Both HPTLC and immunohistochemistry analyses revealed that PAECs incubated with FBS predominantly express the gangliosides GM3, GM1, and GD3. However, the expression of GM1 significantly decreased in PAECs incubated for 5 h with TNF-α (10 ng/mL), 10% human serum containing human leukocytes, and 10% FBS containing human leukocytes. Taken together, these results suggest that human leukocytes induced changes in the expression profile of ganglioside GM1 similar to those seen upon treatment of PAECs with TNF-α. This finding may be relevant for designing future therapeutic strategies intended to prolong xenograft survival.

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