NDLI: ARS-interacting multi-functional protein 1 induces proliferation of human bone marrow-derived mesenchymal stem cells by accumulation of ß-catenin via fibroblast growth factor receptor 2-mediated activation of Akt.

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Epigenetic Regulation of the Electrophysiological Phenotype of Human Embryonic Stem Cell-Derived Ventricular Cardiomyocytes: Insights for Driven Maturation and Hypertrophic Growth

ARS-interacting multi-functional protein 1 induces proliferation of human bone marrow-derived mesenchymal stem cells by accumulation of ß-catenin via fibroblast growth factor receptor 2-mediated activation of Akt.

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Decidual stromal cells promote regulatory T cells and suppress alloreactivity in a cell contact-dependent manner.

Immunological properties of extraembryonic human mesenchymal stromal cells derived from gestational tissue.

Temporal modulation of ß-catenin signaling by multicellular aggregation kinetics impacts embryonic stem cell cardiomyogenesis.

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ARS-interacting multi-functional protein 1 induces proliferation of human bone marrow-derived mesenchymal stem cells by accumulation of ß-catenin via fibroblast growth factor receptor 2-mediated activation of Akt.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Kim, Seo Yoon Son, Woo Sung Park, Min Chul Kim, Chul Min Cha, Byung Hyun Yoon, Kang Jun Lee, Soo-Hong Park, Sang Gyu
Description	Author Affiliation: Kim SY ( 1 Laboratory for Tracing of Gene Function, Department of Biomedical Science, CHA University , Sungnam-si, Korea.)
Abstract	ARS-Interacting Multi-functional Protein 1 (AIMP1) is a cytokine that is involved in the regulation of angiogenesis, immune activation, and fibroblast proliferation. In this study, fibroblast growth factor receptor 2 (FGFR2) was isolated as a binding partner of AIMP peptide (amino acids 6-46) in affinity purification using human bone marrow-derived mesenchymal stem cells (BMMSCs). AIMP1 peptide induced the proliferation of adult BMMSCs by activating Akt, inhibiting glycogen synthase kinase-3ß, and thereby increasing the level of ß-catenin. In addition, AIMP1 peptide induced the translocation of ß-catenin to the nucleus and increased the transcription of c-myc and cyclin D1 by activating the ß-catenin/T-cell factor (TCF) complex. By contrast, transfection of dominant negative TCF abolished the effect of AIMP1. The inhibition of Akt, using LY294002, abolished the accumulation and nuclear translocation of ß-catenin induced by AIMP1, leading to a decrease in c-myc and cyclin D1 expression, which decreased the proliferation of BMMSCs. An intraperitoneal injection of AIMP1 peptide into C57/BL6 mice increased the colony formation of fibroblast-like cells. Fluorescence activated cell sorting analysis showed that the colony-forming cells were CD29(+)/CD44(+)/CD90(+)/CD105(+)/CD34(-)/CD45(-), which is characteristic of MSCs. In addition, the fibroblast-like cells differentiated into adipocytes, chondrocytes, and osteocytes. Taken together, these data suggest that AIMP1 peptide promotes the proliferation of BMMSCs by activating the ß-catenin/TCF complex via FGFR2-mediated activation of Akt, which leads to an increase in MSCs in peripheral blood.
File Format	HTM / HTML
ISSN	15473287
e-ISSN	15578534
DOI	10.1089/scd.2012.0714
Journal	Stem Cells and Development
Issue Number	19
Volume Number	22
Language	English
Publisher	Mary Ann Liebert, Inc.
Publisher Date	2013-10-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Discipline Cell Biology Discipline Hematology Cytokines Metabolism Mesenchymal Stromal Cells Neoplasm Proteins Proto-oncogene Proteins C-akt Rna-binding Proteins Receptor, Fibroblast Growth Factor, Type 2 Beta Catenin Active Transport, Cell Nucleus Adipocytes Animals Bone Marrow Cells Cytology Cell Differentiation Cell Proliferation Cells, Cultured Chondrocytes Chromones Pharmacology Cyclin D1 Biosynthesis Genetics Enzyme Activation Extracellular Signal-regulated Map Kinases Glycogen Synthase Kinase 3 Antagonists & Inhibitors Mice Mice, Inbred C57bl Morpholines Osteocytes Phosphorylation Protein Binding Proto-oncogene Proteins C-myc Tcf Transcription Factors Transcription, Genetic Research Support, Non-u.s. Gov't
Content Type	Text
Resource Type	Article
Subject	Cell Biology Developmental Biology Hematology

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ARS-Interacting Multi-Functional Protein 1 Induces Proliferation of Human Bone Marrow-Derived Mesenchymal Stem Cells by Accumulation of β-Catenin via Fibroblast Growth Factor Receptor 2-Mediated Activation of Akt

Downregulation of ß-catenin and Akt signaling is responsible for poor proliferation of the late passage of bone marrow mesenchymal stem cells.

Signaling from fibroblast growth factor receptor 2 in immature hematopoietic cells facilitates donor hematopoiesis after intra-bone marrow-bone marrow transplantation.

Deficiency of GRP94 in the hematopoietic system alters proliferation regulators in hematopoietic stem cells.

Inhibitory effect of nordihydroguaiaretic acid on ß-catenin/Tcf signalling in ß-catenin-activated cells.

Epithelial Mesenchymal Transition by C-Fos Estrogen Receptor Activation Involves Nuclear Translocation of β-Catenin and Upregulation of β-Catenin/Lymphoid Enhancer Binding Factor-1 Transcriptional Activity

WNT-1 Signaling Inhibits Apoptosis by Activating β-Catenin/T Cell Factor–Mediated Transcription

IL-8 enhances the angiogenic potential of human bone marrow mesenchymal stem cells by increasing vascular endothelial growth factor.

Arachidonoyl-phosphatidylcholine oscillates during the cell cycle and counteracts proliferation by suppressing Akt membrane binding.

ARS-interacting multi-functional protein 1 induces proliferation of human bone marrow-derived mesenchymal stem cells by accumulation of ß-catenin via fibroblast growth factor receptor 2-mediated activation of Akt.

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ARS-Interacting Multi-Functional Protein 1 Induces Proliferation of Human Bone Marrow-Derived Mesenchymal Stem Cells by Accumulation of β-Catenin via Fibroblast Growth Factor Receptor 2-Mediated Activation of Akt

Downregulation of ß-catenin and Akt signaling is responsible for poor proliferation of the late passage of bone marrow mesenchymal stem cells.

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ARS-interacting multi-functional protein 1 induces proliferation of human bone marrow-derived mesenchymal stem cells by accumulation of ß-catenin via fibroblast growth factor receptor 2-mediated activation of Akt.