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Journal articles on the topic 'C3H10T1/2'

Author: Grafiati
Published: 4 June 2021
Last updated: 11 February 2022

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1

Moseti, Dorothy, Alemu Regassa, Chongxiao Chen, Karmin O, and Woo Kyun Kim. "25-Hydroxycholesterol Inhibits Adipogenic Differentiation of C3H10T1/2 Pluripotent Stromal Cells." International Journal of Molecular Sciences 21, no. 2 (2020): 412. http://dx.doi.org/10.3390/ijms21020412.

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Understanding of adipogenesis is important to find remedies for obesity and related disorders. In addition, it is also critical in bone disorders because there is a reciprocal relationship between adipogenesis and osteogenesis in bone micro-environment. Oxysterols are pro-osteogenic and anti-adipogenic molecules via hedgehog activation in pluripotent bone marrow stomal cells. However, no study has evaluated the role of specific oxysterols in C3H10T1/2 cells, which are a good cell model for studying osteogenesis and adipogenesis in bone-marrows. Thus, we investigated the effects of specific oxysterols on adipogenesis and expression of adipogenic transcripts in C3H10T1/2 cells. Treatment of cells with DMITro significantly induced mRNA expression of Pparγ. This induction was significantly inhibited by 25-HC. The expression of C/cepα, Fabp4 and Lpl was also inhibited by 25-HC. To determine the mechanism by which 25-HC inhibits adipogenesis, the effects of the hedgehog signalling pathway inhibitor, cyclopamine and CUR61414, were evaluated. Treatment of C3H10T1/2 cells with DMITro + cyclopamine or DMITro + CUR61414 for 96h did not modulate adipocyte differentiation; cyclopamine and CUR61414 did not reverse the inhibitory effects of 25-HC, suggesting that the canonical hedgehog signalling may not play a role in the anti-adipogenic effects of 25-HC in C3H10T1/2 cells. In addition, LXR agonist did not inhibit adipogenesis, but 25-HC strongly inhibits adipogenesis of C3H10T1/2 cells. Our observations showed that 25-HC was the most potent oxysterol in inhibiting adipogenesis and the expression of key adipogenic transcripts in C3H10T1/2 cells among the tested oxysterols, suggesting its potential application in providing an intervention in osteoporosis and obesity. We also report that the inhibitory effects of 25-HC on adipogenic differentiation in C3H10T1/2 cells are not mediated by hedgehog signaling and LXR.
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2

Wang, Xueyan, Mette A. Peters, Fransiscus E. Utama, Yuzhen Wang, and Elizabeth J. Taparowsky. "The Adrenomedullin Gene Is a Target for Negative Regulation by the Myc Transcription Complex." Molecular Endocrinology 13, no. 2 (1999): 254–67. http://dx.doi.org/10.1210/mend.13.2.0240.

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Abstract The Myc family of transcription factors plays a central role in vertebrate growth and development although relatively few genetic targets of the Myc transcription complex have been identified. In this study, we used mRNA differential display to investigate gene expression changes induced by the overexpression of the MC29 v-Myc oncoprotein in C3H10T1/2 mouse fibroblasts. We identified the transcript of the adrenomedullin gene (AM) as an mRNA that is specifically down-regulated in v-Myc overexpressing C3H10T1/2 cell lines as well as in a Rat 1a cell line inducible for c-Myc. Nucleotide sequence analysis of the mouse AM promoter reveals the presence of consensus CAAT and TATA boxes as well as an initiator element (INR) with significant sequence similarity to the INR responsible for Myc-mediated repression of the adenovirus major late promoter (AdMLP). Reporter gene assays confirm that the region of the AM promoter containing the INR is the target of Myc-mediated repression. Exogenous application of AM peptide to quiescent C3H10T1/2 cultures does not stimulate growth, and constitutive expression of AM mRNA in C3H10T1/2 cells correlates with a reduced potential of the cells to be cotransformed by v-Myc and oncogenic Ras p21. Additional studies showing that AM mRNA is underrepresented in C3H10T1/2 cell lines stably transformed by Ras p21 or adenovirus E1A suggest that AM gene expression is incompatible with deregulated growth in this cell line. We propose a model in which the repression of AM gene expression by Myc is important to the role of this oncoprotein as a potentiator of cellular transformation in C3H10T1/2 and perhaps other cell lines.
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3

Zhao, Mingyan, Reema Anouz, and Thomas Groth. "Effect of microenvironment on adhesion and differentiation of murine C3H10T1/2 cells cultured on multilayers containing collagen I and glycosaminoglycans." Journal of Tissue Engineering 11 (January 2020): 204173142094056. http://dx.doi.org/10.1177/2041731420940560.

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Polyelectrolyte multilayer coating is a promising tool to control cellular behavior. Murine C3H10T1/2 embryonic fibroblasts share many features with mesenchymal stem cells, which are good candidates for use in regenerative medicine. However, the interactions of C3H10T1/2 cells with polyelectrolyte multilayers have not been studied yet. Hence, the effect of molecular composition of biomimetic multilayers, by pairing collagen I (Col I) with either hyaluronic acid or chondroitin sulfate, based primarily on ion pairing and on additional intrinsic cross-linking was studied regarding the adhesion and differentiation of C3H10T1/2 cells. It was found that the adhesion and osteogenic differentiation of C3H10T1/2 cells were more pronounced on chondroitin sulfate-based multilayers when cultured in the absence of osteogenic supplements, which corresponded to the significant larger amounts of Col I fibrils in these multilayers. By contrast, the staining of cartilage-specific matrixes was more intensive when cells were cultured on hyaluronic acid-based multilayers. Moreover, it is of note that a limited osteogenic and chondrogenic differentiation were detected when cells were cultured in osteogenic or chondrogenic medium. Specifically, cells were largely differentiated into an adipogenic lineage when cultured in osteogenic medium or 100 ng mL−1 bone morphogenic protein 2, and it was more evident on the oxidized glycosaminoglycans-based multilayers, which corresponded also to the higher stiffness of cross-linked multilayers. Overall, polyelectrolyte multilayer composition and stiffness can be used to direct cell–matrix interactions, and hence the fate of C3H10T1/2 cells. However, these cells have a higher adipogenic potential than osteogenic or chondrogenic potential.
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4

Hoffmann, Andrea, Stefan Czichos, Christian Kaps, et al. "The T-box transcription factor Brachyury mediates cartilage development in mesenchymal stem cell line C3H10T1/2." Journal of Cell Science 115, no. 4 (2002): 769–81. http://dx.doi.org/10.1242/jcs.115.4.769.

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The BMP2-dependent onset of osteo/chondrogenic differentiation in the acknowledged pluripotent murine mesenchymal stem cell line (C3H10T1/2) is accompanied by the immediate upregulation of Fibroblast Growth Factor Receptor 3 (FGFR3) and a delayed response by FGFR2. Forced expression of FGFR3 in C3H10T1/2 is sufficient for chondrogenic differentiation, indicating an important role for FGF-signaling during the manifestation of the chondrogenic lineage in this cell line. Screening for transcription factors exhibiting a chondrogenic capacity in C3H10T1/2 indentified that the T-box containing transcription factor Brachyury is upregulated by FGFR3-mediated signaling. Forced expression of Brachyury in C3H10T1/2 was sufficient for differentiation into the chondrogenic lineage in vitro and in vivo after transplantation into muscle. A dominant-negative variant of Brachyury, consisting of its DNA-binding domain (T-box), interferes with BMP2-mediated cartilage formation. These studies indicate that BMP-initiated FGF-signaling induces a novel type of transcription factor for the onset of chondrogenesis in a mesenchymal stem cell line. A potential role for this T-box factor in skeletogenesis is further delineated from its expression profile in various skeletal elements such as intervertebral disks and the limb bud at late stages (18.5 d.p.c.) of murine embryonic development.
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5

Rodríguez-Cano, María-Milagros, María-Julia González-Gómez, Beatriz Sánchez-Solana, et al. "NOTCH Receptors and DLK Proteins Enhance Brown Adipogenesis in Mesenchymal C3H10T1/2 Cells." Cells 9, no. 9 (2020): 2032. http://dx.doi.org/10.3390/cells9092032.

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The NOTCH family of receptors and ligands is involved in numerous cell differentiation processes, including adipogenesis. We recently showed that overexpression of each of the four NOTCH receptors in 3T3-L1 preadipocytes enhances adipogenesis and modulates the acquisition of the mature adipocyte phenotype. We also revealed that DLK proteins modulate the adipogenesis of 3T3-L1 preadipocytes and mesenchymal C3H10T1/2 cells in an opposite way, despite their function as non-canonical inhibitory ligands of NOTCH receptors. In this work, we used multipotent C3H10T1/2 cells as an adipogenic model. We used standard adipogenic procedures and analyzed different parameters by using quantitative-polymerase chain reaction (qPCR), quantitative reverse transcription-polymerase chain reaction (qRT-PCR), luciferase, Western blot, and metabolic assays. We revealed that C3H10T1/2 multipotent cells show higher levels of NOTCH receptors expression and activity and lower Dlk gene expression levels than 3T3-L1 preadipocytes. We found that the overexpression of NOTCH receptors enhanced C3H10T1/2 adipogenesis levels, and the overexpression of NOTCH receptors and DLK (DELTA-like homolog) proteins modulated the conversion of cells towards a brown-like adipocyte phenotype. These and our prior results with 3T3-L1 preadipocytes strengthen the idea that, depending on the cellular context, a precise and highly regulated level of global NOTCH signaling is necessary to allow adipogenesis and determine the mature adipocyte phenotype.
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Hata, Kenji, Riko Nishimura, Fumiyo Ikeda та ін. "Differential Roles of Smad1 and p38 Kinase in Regulation of Peroxisome Proliferator-activating Receptor γ during Bone Morphogenetic Protein 2-induced Adipogenesis". Molecular Biology of the Cell 14, № 2 (2003): 545–55. http://dx.doi.org/10.1091/mbc.e02-06-0356.

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Bone morphogenetic protein 2 (BMP2) promotes the differentiation of undifferentiated mesenchymal cells into adipocytes. To investigate the molecular mechanisms that regulate this differentiation process, we studied the relationship between BMP2 signaling and peroxisome proliferator-activating receptor γ (PPARγ) during adipogenesis of mesenchymal cells by using pluripotent mesenchymal cell line C3H10T1/2. In C3H10T1/2 cells, BMP2 induced expression of PPARγ along with adipogenesis. Overexpression of Smad6, a natural antagonist for Smad1, blocked PPARγ expression and adipocytic differentiation induced by BMP2. Overexpression of dominant-negative PPARγ also diminished adipocytic differentiation of C3H10T1/2 cells, suggesting the central role of PPARγ in BMP2-induced adipocytic differentiation. Specific inhibitors for p38 kinase inhibited BMP2-induced adipocytic differentiation and transcriptional activation of PPARγ, whereas overexpression of Smad6 had no effect on transcriptional activity of PPARγ. Furthermore, activation of p38 kinase by overexpression of TAK1 and TAB1, without affecting PPARγ expression, led the up-regulation of transcriptional activity of PPARγ. These results suggest that both Smad and p38 kinase signaling are concomitantly activated and responsible for BMP2-induced adipocytic differentiation by inducing and up-regulating PPARγ, respectively. Thus, BMP2 controls adipocytic differentiation by using two distinct signaling pathways that play differential roles in this process in C3H10T1/2 cells.
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7

Ogawa, Akira, Ken-Ichi Ohba, Yoko Uchida, Keiji Wada, Toshimasa Yoshioka, and Takamura Muraki. "New adipogenic cell lines derived from C3H10T1/2." In Vitro Cellular & Developmental Biology - Animal 35, no. 6 (1999): 307–10. http://dx.doi.org/10.1007/s11626-999-0078-5.

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8

Takami, Akiko, Hirotaka Kato, Ryousuke Takagi, and Tomoyuki Miyashita. "Studies on thePinctada fucataBMP-2 Gene: Structural Similarity and Functional Conservation of Its Osteogenic Potential within the Animal Kingdom." International Journal of Zoology 2013 (2013): 1–9. http://dx.doi.org/10.1155/2013/787323.

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Bone morphogenetic protein (BMP)-2 plays an important role in morphogenesis in both vertebrates and invertebrates. BMP-2 is one of the most powerful bioactive substances known to induce the osteogenic differentiation of mesenchymal cells. We examined the structural and functional conservation ofPinctada fucataBMP-2 in inducing osteogenesis in the murine mesenchymal stem cells, C3H10T1/2. Exposure of C3H10T1/2 cells to the recombinant mature fragment ofPinctada fucataBMP-2 resulted in osteoblastic differentiation. The sequence, SVPKPCCVPTELSSL, within the C-terminal portion ofPinctada fucataBMP-2, is homologous to the knuckle epitope of human BMP-2. This synthetic polypeptide was able to induce differentiation of C3H10T1/2 along the osteoblastic lineage, as confirmed by an increase in alkaline phosphatase activity, and the accumulation of calcium, as determined by von Kossa staining. Furthermore, using immunohistochemical staining, we observed an increased expression of collagen type I, osteopontin, and osteocalcin, which are known markers of osteogenesis. These results show that BMP-2 is conserved, not only in terms of its homology at the amino acid sequence, but also in terms of driving the formation of hard tissues in vertebrates and invertebrates.
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9

Lin, Li Wen, King L. Chow, and Yang Leng. "Study of Hydroxyapatite Osteoinduction with Osteo-Specific Gene Expression of Stem Cells." Key Engineering Materials 361-363 (November 2007): 1005–8. http://dx.doi.org/10.4028/www.scientific.net/kem.361-363.1005.

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Osteoinductivity of hydroxyapatite (HA) was investigated using uncommitted pluripotent mouse stem cells, C3H10T1/2 in an in vitro differentiation assay. HA exhibited impressive ability to induce expression of osteo-specific genes in C3H10T1/2, including alkaline phosphatase (ALP), type I collagen (COL1) and osteocalcin (OCN); compared with its insignificant up-regulation of the same genes in osteoblast-like cells, Saos-2. HA osteoinductivity exhibited in C3H10T1/2 was comparable to that of a bone morphogenetic protein (BMP) with reference to up-regulating osteo-specific genes except the core binding factor 1 (Cbfa1, Runx). This result implies a difference in osteogenic induction pathway initiated by HA and BMP. HA osteoinductivity was also demonstrated in the stem cells culture using conditioned medium derived from cells cultured on HA substrates. The medium exhibited excellent ability to up-regulate ALP without the presence of HA and BMP. The result suggests that the HA can interact with the cells and generate potent inductive substance released into the medium. Such substance in turn is able to induce uncommitted cells to differentiate into the osteolineage.
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10

Waligorski, M. P. R., G. L. Sinclair, and R. Katz. "Radiosensitivity Parameters for Neoplastic Transformations in C3H10T1/2 Cells." Radiation Research 111, no. 3 (1987): 424. http://dx.doi.org/10.2307/3576928.

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11

Maudsley, D. J., and A. G. Morris. "Kirsten murine sarcoma virus abolishes interferon gamma-induced class II but not class I major histocompatibility antigen expression in a murine fibroblast line." Journal of Experimental Medicine 167, no. 2 (1988): 706–11. http://dx.doi.org/10.1084/jem.167.2.706.

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The effect of infecting fibroblasts with Kirsten murine sarcoma virus/murine leukemia virus (Ki-MSV/MLV) on constitutive and IFN-gamma-induced H-2 antigen expression was investigated. The fibroblasts used were two established cell lines (C3H10T1/2 and BALB/c3T3) and fresh embryo fibroblasts from C3H mice. Class I antigens were expressed constitutively by BALB/c3T3; infection with MLV, MSV or the two together had little effect on this constitutive expression. Class I antigens (H-2K, H-2D) were strongly induced on all three types of fibroblast by rIFN-gamma, and infection had little effect on this. None of the fibroblasts expressed constitutively detectable levels of class II antigen; however, C3H10T1/2 fibroblasts could be induced for both H-2A and H-2E by IFN-gamma. Infection of C3H10T1/2 with helper-free Ki-MSV, or MSV together with MLV, completely abolished this induction of class II antigens, while infection with MLV alone had little effect, implying that the abolition of class II induction was due to genomic regions of Ki-MSV not shared with Ki-MLV, probably the v-Ki-ras gene.
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12

Spinella-Jaegle, Sylviane, Georges Rawadi, Shinji Kawai, et al. "Sonic hedgehog increases the commitment of pluripotent mesenchymal cells into the osteoblastic lineage and abolishes adipocytic differentiation." Journal of Cell Science 114, no. 11 (2001): 2085–94. http://dx.doi.org/10.1242/jcs.114.11.2085.

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The proteins of the hedgehog (Hh) family regulate various aspects of development. Recently, members of this family have been shown to regulate skeletal formation in vertebrates and to control both chondrocyte and osteoblast differentiation. In the present study, we analyzed the effect of Sonic hedgehog (Shh) on the osteoblastic and adipocytic commitment/differentiation. Recombinant N-terminal Shh (N-Shh) significantly increased the percentage of both the pluripotent mesenchymal cell lines C3H10T1/2 and ST2 and calvaria cells responding to bone morphogenetic protein 2 (BMP-2), in terms of osteoblast commitment as assessed by measuring alkaline phosphatase (ALP) activity. This synergistic effect was mediated, at least partly, through the positive modulation of the transcriptional output of BMPs via Smad signaling. Furthermore, N-Shh was found to abolish adipocytic differentiation of C3H10T1/2 cells both in the presence or absence of BMP-2. A short treatment with N-Shh was sufficient to dramatically reduce the levels of the adipocytic-related transcription factors C/EBPα and PPARγ in both C3H10T1/2 and calvaria cell cultures. Given the inverse relationship between marrow adipocytes and osteoblasts with aging, agonists of the Hh signaling pathway might constitute potential drugs for preventing and/or treating osteopenic disorders.
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13

C. Miller, S. A. Marino, J. Napoli,, R. "Oncogenic transformation in C3H10T1/2 cells by low-energy neutrons." International Journal of Radiation Biology 76, no. 3 (2000): 327–33. http://dx.doi.org/10.1080/095530000138664.

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14

Williams, K. P., P. Rayhorn, G. Chi-Rosso, et al. "Functional antagonists of sonic hedgehog reveal the importance of the N terminus for activity." Journal of Cell Science 112, no. 23 (1999): 4405–14. http://dx.doi.org/10.1242/jcs.112.23.4405.

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During development, sonic hedgehog functions as a morphogen in both a short-range contact-dependent and in a long-range diffusable mode. Here, we show using a panel of sonic hedgehog variants that regions near the N terminus of the protein play a critical role in modulating these functions. In the hedgehog responsive cell line C3H10T1/2, we discovered that not only were some N-terminally truncated variants inactive at eliciting a hedgehog-dependent response, but they competed with the wild-type protein for function and therefore served as functional antagonists. These variants were indistinguishable from wild-type sonic hedgehog in their ability to bind the receptor patched-1, but failed to induce the hedgehog-responsive markers, Gli-1 and Ptc-1, and failed to promote hedgehog-dependent differentiation of the cell line. They also failed to support the adhesion of C3H10T1/2 cells to hedgehog-coated plates under conditions where wild-type sonic hedgehog supported binding. Structure-activity data indicated that the N-terminal cysteine plays a key regulatory role in modulating hedgehog activity. The ability to dissect patched-1 binding from signaling events in C3H10T1/2 cells suggests the presence of unidentified factors that contribute to hedgehog responses.
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15

Mie, Masayasu, Hajime Ohgushi, Yasuko Yanagida, Tetsuya Haruyama, Eiry Kobatake, and Masuo Aizawa. "Osteogenesis Coordinated in C3H10T1/2 Cells by Adipogenesis-Dependent BMP-2 Expression System." Tissue Engineering 6, no. 1 (2000): 9–18. http://dx.doi.org/10.1089/107632700320847.

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16

Oh, I., K. Ozaki, A. Miyazato, et al. "Screening of genes responsible for differentiation of mouse mesenchymal stromal cells by DNA micro-array analysis of C3H10T1/2 and C3H10T1/2-derived cell lines." Cytotherapy 9, no. 1 (2007): 80–90. http://dx.doi.org/10.1080/14653240601016374.

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17

Li, Mingshan, Zijie Pei, Hongtao Zhang, and Jing Qu. "Expression Profile of Long Noncoding RNAs and Circular RNAs in Mouse C3H10T1/2 Mesenchymal Stem Cells Undergoing Myogenic and Cardiomyogenic Differentiation." Stem Cells International 2021 (April 30, 2021): 1–21. http://dx.doi.org/10.1155/2021/8882264.

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Background. Currently, a heterogeneous category of noncoding RNAs (ncRNA) that directly regulate the expression or function of protein-coding genes is shown to have an effect on the fate decision of stem cells. However, the detailed regulatory roles of ncRNAs in myogenic and cardiomyogenic differentiation of mouse C3H10T1/2 mesenchymal stem cells (MSCs) are far from clear. Methods. In this study, 5-azacytidine- (5-AZA-) treated C3H10T1/2 cells were differentiated into myocyte-like and cardiomyocyte-like cells. Next, ncRNA associated with myogenic and cardiomyogenic differentiation was identified using high-throughput RNA sequencing (RNA-seq) data. Bioinformatics analysis was conducted to identify the differentially expressed ncRNAs and the related signaling pathways. Results. Myotube-like structure was formed after 5-AZA treatment of C3H10T1/2 cells. In addition, myogenic and cardiomyogenic differentiation-related genes like GATA4, cTnt, MyoD, and Desmin were upregulated significantly after the 5-AZA treatment. Totally, 1538 differentially expressed lncRNAs and 3398 differentially expressed mRNAs were identified, including 1175 upregulated and 363 downregulated lncRNAs and 2429 upregulated and 969 downregulated mRNAs. In addition, 46 differentially expressed circRNAs were identified, including 25 upregulated and 21 downregulated circRNAs. Moreover, the differentially expressed mRNAs were enriched into 5 significant pathways, including those for focal adhesion, ECM-receptor interaction, PI3K-AKT signaling pathway, PPAR signaling pathway, and Tyrosine metabolism. Conclusions. A systematic view of the expression of ncRNAs in myogenic and cardiomyogenic differentiation of MSCs was provided in the study.
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18

Lautier, Dominique, Danièle Poirier, Annie Boudreau, Moulay A. Alaoui Jamali, André Castonguay, and Guy Poirier. "Stimulation of poly(ADP-ribose) synthesis by free radicals in C3H10T1/2 cells: relationship with NAD metabolism and DNA breakage." Biochemistry and Cell Biology 68, no. 3 (1990): 602–8. http://dx.doi.org/10.1139/o90-085.

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We have studied the effect of H2O2 and O2− produced by xanthine and xanthine oxidase on NAD catabolism, poly(ADP-ribose) synthesis, and production of DNA single-strand breaks in C3H10T1/2 cells. The results show a correlation between the induction of DNA single-strand breaks, the decrease of NAD pool, and the accumulation of polymer. New techniques, based on affinity chromatography and reversed-phase high pressure liquid chromatography, have allowed an accurate determination of polymer contents and showed a 20-fold stimulation of polymer biosynthesis induced by active oxygen species. Inhibition experiments performed with 3-aminobenzamide have shown that the decrease in NAD levels after exposure of cells to active oxygen species was caused by stimulation of poly(ADP-ribosyl)ation and of another cellular process.Key words: poly(ADP-ribose), free radicals, C3H10T1/2 cells, DNA breakage, NAD catabolism.
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19

Ramaraj, Pandurangan, Jorge N. Artaza, Indrani Sinha-Hikim, and Wayne E. Taylor. "Effect of Androstenedione on Adipogenesis in Murine C3H10T1/2 Mesenchymal Cells." Open Journal of Endocrine and Metabolic Diseases 05, no. 02 (2015): 9–18. http://dx.doi.org/10.4236/ojemd.2015.52002.

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20

Sugatani, T., M. Nakase, Y. Kurita, M. Hashimoto, H. Kihira, and T. Tagawa. "Cyclic nucleotide phosphodiesterases in the osteoblastic differentiation of C3H10T1/2 cells." International Journal of Oral and Maxillofacial Surgery 26 (January 1997): 170–71. http://dx.doi.org/10.1016/s0901-5027(97)81352-5.

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21

Herschman, H., and D. Brankow. "Ultraviolet irradiation transforms C3H10T1/2 cells to a unique, suppressible phenotype." Science 234, no. 4782 (1986): 1385–88. http://dx.doi.org/10.1126/science.3787250.

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Tang, Q. Q., T. C. Otto, and M. D. Lane. "Commitment of C3H10T1/2 pluripotent stem cells to the adipocyte lineage." Proceedings of the National Academy of Sciences 101, no. 26 (2004): 9607–11. http://dx.doi.org/10.1073/pnas.0403100101.

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23

Saran, A., S. Pazzaglia, S. Rebessi, and L. Pariset. "A Freezing Technique Applicable to Transformation Studies of C3H10T1/2 Cells." International Journal of Radiation Biology 61, no. 4 (1992): 545–47. http://dx.doi.org/10.1080/09553009214551311.

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BETTEGA P. CALZOLARI R. MARCHESINI, D. "Inactivation of C3H10T1/2 cells by low energy protons and deuterons." International Journal of Radiation Biology 73, no. 3 (1998): 303–9. http://dx.doi.org/10.1080/095530098142400.

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25

Ker, Dai Fei Elmer, Rashmi Sharma, Evelyna Tsi Hsin Wang, and Yunzhi Peter Yang. "Development of mRuby2-Transfected C3H10T1/2 Fibroblasts for Musculoskeletal Tissue Engineering." PLOS ONE 10, no. 9 (2015): e0139054. http://dx.doi.org/10.1371/journal.pone.0139054.

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Bettega, D., P. Calzolari, A. Ottolenghi, and L. Tallone Lombardi. "Growth Kinetics of C3H10T1/2 Cells Exposed to Low-LET Radiation." International Journal of Radiation Biology 55, no. 4 (1989): 641–51. http://dx.doi.org/10.1080/09553008914550681.

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27

Taira, M., M. S. Toguchi, Y. Hamada, et al. "Studies on cytotoxicity of nickel ions using C3H10T1/2 fibroblast cells." Journal of Oral Rehabilitation 27, no. 12 (2000): 1068–72. http://dx.doi.org/10.1046/j.1365-2842.2000.00608.x.

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Ogino, Yoichiro, Ruiwei Liang, Daniela B. S. Mendonça, et al. "RhoA-Mediated Functions in C3H10T1/2 Osteoprogenitors Are Substrate Topography Dependent." Journal of Cellular Physiology 231, no. 3 (2015): 568–75. http://dx.doi.org/10.1002/jcp.25100.

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Taira, M., M. S. Toguchi, Y. Hamada, et al. "Studies on cytotoxicity of nickel ions using C3H10T1/2 fibroblast cells." Journal of Oral Rehabilitation 27, no. 12 (2008): 1068–72. http://dx.doi.org/10.1111/j.1365-2842.2000.00608.x.

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30

Gomes, Ronald R., Sonali S. Joshi, Mary C. Farach-Carson, and Daniel D. Carson. "Ribozyme-mediated perlecan knockdown impairs chondrogenic differentiation of C3H10T1/2 fibroblasts." Differentiation 74, no. 1 (2006): 53–63. http://dx.doi.org/10.1111/j.1432-0436.2005.00055.x.

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Jackson, Amanda, Béatrice Vayssière, Teresa Garcia, et al. "Gene array analysis of Wnt-regulated genes in C3H10T1/2 cells." Bone 36, no. 4 (2005): 585–98. http://dx.doi.org/10.1016/j.bone.2005.01.007.

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32

Jian, Ruo-Lei, Li-Bin Mao, Yao Xu, et al. "Generation of insulin-producing cells from C3H10T1/2 mesenchymal progenitor cells." Gene 562, no. 1 (2015): 107–16. http://dx.doi.org/10.1016/j.gene.2015.02.061.

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Hashimoto, Yoko, Etsuko Matsuzaki, Katsumasa Higashi, et al. "Sphingosine-1-phosphate inhibits differentiation of C3H10T1/2 cells into adipocyte." Molecular and Cellular Biochemistry 401, no. 1-2 (2014): 39–47. http://dx.doi.org/10.1007/s11010-014-2290-1.

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Harrington, M. A., J. H. Falkenburg, R. Daub, and H. E. Broxmeyer. "Effect of myogenic and adipogenic differentiation on expression of colony-stimulating factor genes." Molecular and Cellular Biology 10, no. 9 (1990): 4948–52. http://dx.doi.org/10.1128/mcb.10.9.4948.

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The influence of cellular differentiation on colony-stimulating factor gene expression was examined in myogenically and adipogenically determined cell lines derived from 5-azacytidine-treated C3H10T1/2 C18 (10T1/2) mouse embryo fibroblasts. These studies demonstrate that colony-stimulating factor gene expression can be modulated by myogenic and adipogenic determination and terminal differentiation.
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Harrington, M. A., J. H. Falkenburg, R. Daub, and H. E. Broxmeyer. "Effect of myogenic and adipogenic differentiation on expression of colony-stimulating factor genes." Molecular and Cellular Biology 10, no. 9 (1990): 4948–52. http://dx.doi.org/10.1128/mcb.10.9.4948-4952.1990.

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The influence of cellular differentiation on colony-stimulating factor gene expression was examined in myogenically and adipogenically determined cell lines derived from 5-azacytidine-treated C3H10T1/2 C18 (10T1/2) mouse embryo fibroblasts. These studies demonstrate that colony-stimulating factor gene expression can be modulated by myogenic and adipogenic determination and terminal differentiation.
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36

Komatsu, Kenshi, Yutaka Okumura, and Seiji Kodama. "The Oncogenic Potential of Thermotolerant C3H10T 1/2 Cells." Thermal Medicine(Japanese Journal of Hyperthermic Oncology) 4, no. 4 (1988): 265–71. http://dx.doi.org/10.3191/thermalmedicine.4.265.

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Cheng, Kur-Ta, Yu-Shiou Wang, Hsiu-Chu Chou, Chih-Cheng Chang, Ching-Kuo Lee, and Shu-Hui Juan. "Kinsenoside-mediated lipolysis through an AMPK-dependent pathway in C3H10T1/2 adipocytes." Phytomedicine 22, no. 6 (2015): 641–47. http://dx.doi.org/10.1016/j.phymed.2015.04.001.

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Takata, Tomoyo, and Chie Morimoto. "Raspberry Ketone Promotes the Differentiation of C3H10T1/2 Stem Cells into Osteoblasts." Journal of Medicinal Food 17, no. 3 (2014): 332–38. http://dx.doi.org/10.1089/jmf.2013.2763.

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Chen, Anne C., David W. Brankow, and Harvey R. Herschman. "A reassessment of methylcholanthrene transformation in the C3H10T1/2 cell culture system." Carcinogenesis 11, no. 5 (1990): 817–22. http://dx.doi.org/10.1093/carcin/11.5.817.

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Bostr�m, Kristina, Yin Tintut, Shih Chi Kao, William P. Stanford, and Linda L. Demer. "HOXB7 overexpression promotes differentiation of C3H10T1/2 cells to smooth muscle cells." Journal of Cellular Biochemistry 78, no. 2 (2000): 210–21. http://dx.doi.org/10.1002/(sici)1097-4644(20000801)78:2<210::aid-jcb4>3.0.co;2-z.

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Crowe, R. A., E. J. Taparowsky, and F. L. Crane. "Ha-ras Stimulates the Transplasma Membrane Oxidoreductase Activity of C3H10T1/2 Cells." Biochemical and Biophysical Research Communications 196, no. 2 (1993): 844–50. http://dx.doi.org/10.1006/bbrc.1993.2326.

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Zamboni, M., E. Privitera, G. Mosna, and A. Ghidoni. "Sister chromatid exchange in methotrexate resistant and sensitive C3H10T1/2 mouse cells." Genetica 80, no. 3 (1990): 229–33. http://dx.doi.org/10.1007/bf00137330.

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Hashimoto, Yoko, Mari Kobayashi, Etsuko Matsuzaki, et al. "Sphingosine-1-phosphate-enhanced Wnt5a promotes osteogenic differentiation in C3H10T1/2 cells." Cell Biology International 40, no. 10 (2016): 1129–36. http://dx.doi.org/10.1002/cbin.10652.

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Zhang, W. J., B. G. Li, C. Zhang, X. H. Xie, and T. T. Tang. "Biocompatibility and membrane strength of C3H10T1/2 cell-loaded alginate-based microcapsules." Cytotherapy 10, no. 1 (2008): 90–97. http://dx.doi.org/10.1080/14653240701762372.

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Takahashi, Yutaka, Yasuhiko Okimura, Ishikazu Mizuno, et al. "Leptin Induces Mitogen-activated Protein Kinase- dependent Proliferation of C3H10T1/2 Cells." Journal of Biological Chemistry 272, no. 20 (1997): 12897–900. http://dx.doi.org/10.1074/jbc.272.20.12897.

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Roy, Rani, Valery Kudryashov, Stephen B. Doty, Itzhak Binderman, and Adele L. Boskey. "Differentiation and mineralization of murine mesenchymal C3H10T1/2 cells in micromass culture." Differentiation 79, no. 4-5 (2010): 211–17. http://dx.doi.org/10.1016/j.diff.2010.03.003.

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Yoshinobu, Kubota, Inoue Hiroko, and Yoshioka Tohru. "Increased labelling of polyphosphoinositide in chemically transformed cell line C3H10T1/2 CL8." Biochimica et Biophysica Acta (BBA) - Lipids and Lipid Metabolism 875, no. 1 (1986): 1–5. http://dx.doi.org/10.1016/0005-2760(86)90003-2.

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Ogura, Kiyoshi, Yuko S. Niino, and Tadashi Tai. "Galactosylceramide expression factor-1 induces myogenesis in MDCK and C3H10T1/2 cells." Archives of Biochemistry and Biophysics 426, no. 2 (2004): 279–85. http://dx.doi.org/10.1016/j.abb.2004.02.029.

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Yeh, Chien-Yang, Hsin-Ming Chen, Mei-Chi Chang, et al. "Cytotoxicity and transformation of C3H10T1/2 cells induced by areca nut components." Journal of the Formosan Medical Association 115, no. 2 (2016): 108–12. http://dx.doi.org/10.1016/j.jfma.2015.01.004.

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Cappato, Serena, Francesca Giacopelli, Laura Tonachini, Roberto Ravazzolo, and Renata Bocciardi. "Identification of reference genes for quantitative PCR during C3H10T1/2 chondrogenic differentiation." Molecular Biology Reports 46, no. 3 (2019): 3477–85. http://dx.doi.org/10.1007/s11033-019-04713-x.

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