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Dissertations / Theses on the topic 'C3H10T1/2'

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1

Jia, Dan. "Roles of growth hormone in liver growth and mesenchymal stem cell myogenic and adipogenic lineage commitment." Thesis, Virginia Tech, 2013. http://hdl.handle.net/10919/23924.

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Growth hormone (GH) has growth-stimulating effects on skeletal muscle and liver but a growth-inhibitory effect on adipose tissue. The mechanisms underlying these actions of GH are not fully understood. Two studies were conducted to achieve the following objectives: 1) to determine the cellular mechanism by which GH stimulates liver growth; 2) to determine the effects of GH on the commitment of mesenchymal stem cells (MSCs) to myogenic and adipogenic lineages. In the first study, the GH-deficient lit/lit male mice were injected (s.c.) daily with rbGH or vehicle for two weeks. GH-injected lit/lit mice tended to have a greater liver/body weight percentage than lit/lit control mice. GH injection did not alter the percentage of proliferating cells in the liver. However, GH-injected lit/lit mice had 18% larger hepatocytes and 16% less DNA per unit liver weight than those of lit/lit control mice. These data together indicate that GH stimulates liver growth in mice by increasing the size, not by increasing the number of hepatocytes. In the second study, we treated the MSC cell line C3H10T1/2 cells with or without 5'-azacytidine and rbGH for 4 days. We assessed the myogenic or adipogenic potential by determining the ability of these cells to differentiate into myotubes or adipocytes, respectively. C3H10T1/2 cells treated with 5'-azacytidine and GH formed more myotubes, myoblasts, and fewer adipocytes compared to cells treated with 5'-azacytidine alone. Taken together, these results suggest that GH enhances 5'-azacytidine-induced myogenic commitment but inhibits 5'-azacytidine-induced adipogenic commitment in C3H10T1/2 cells.<br>Master of Science
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2

Sjostrom, Danen S. "Wnt Signaling During Inflammation, Mechanical Stimulation and Differentiation." The Ohio State University, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=osu1276121542.

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3

Kaps, Christian. "Die Rolle von Bone-morphogenetic-Protein-Typ-I-Rezeptoren in der Bone-morphogenetic-Protein-2 abhängigen chondro- osteogenen Differenzierung der mesenchymalen Vorläuferzellinie C3H10T1/2." [S.l.] : [s.n.], 2000. http://deposit.ddb.de/cgi-bin/dokserv?idn=960084479.

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4

Wenjun, Ju [Verfasser], and Gerhard [Akademischer Betreuer] Gross. "The role of the signaling mediator Smad1 in BMP2-dependent osteo/chondrogenic development in mesenchymal progenitors (C3H10T1/2) / Ju Wenjun ; Betreuer: Gerhard Gross." Braunschweig : Technische Universität Braunschweig, 1999. http://d-nb.info/1175832502/34.

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5

Gaut, Ludovic. "Mechanical and molecular signals underlying tendon cell differentiation." Electronic Thesis or Diss., Sorbonne université, 2018. http://www.theses.fr/2018SORUS301.

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Les tendons sont une forme unique de tissu conjonctif au sein du système musculosquelettique. Le développement, l’homéostasie et la réparation du tendon reposent sur des combinaisons de paramètres moléculaires et aussi mécaniques, régulant la production et l’assemblage des fibres de collagène. Notre objectif est de comprendre quelles sont les voies de mécanotransduction impliquées dans la différentiation tendineuse, via deux (co-)facteurs de transcription : EGR1 et YAP. Nous avons montré que l’expression du gène de tendon SCX, de EGR1 et l'activité de YAP sont réduites dans les tendons de membres de fœtus de poulet immobilisés. De plus, la reprise des contractions musculaires entraîne une reprise de l’expression des gènes de tendon comparable à celle des fœtus jamais immobilisés. La mécanobiologie du tendon a été étudiée avec des constructions cellulaires en 3-dimensions (3D) en gel de fibrine ou de collagène, faits de cellules souches mésenchymateuses. La perte de tension de ces constructions a induit une chute de l’expression de Egr1, des gènes de tendon et de l’activité de YAP. Une surexpression de Egr1 dans les constructions 3D en gel de fibrine sans tension a empêché la chute d’expression des gènes de tendon. L’activité de YAP et l’expression de Scx ont augmenté en étirant les constructions en gel de collagène. L’inactivation de l’activité de YAP par traitement à la verteporfin (VTPF) a induit une diminution de l’expression des gènes de tendon, qui n’a pas été restaurée lorsque ces constructions traitées ont été étirées. Ensemble, ces résultats montrent l’importance de YAP et EGR1 en aval des signaux mécaniques pour réguler la différentiation des cellules du tendon<br>Tendons are unique forms of connective tissue of the musculoskeletal system. Tendon development, homeostasis and repair rely on specific combinations of mechanical and molecular factors regulating the production and assembly of collagen fibers. Our objective is to decipher the mechanotransduction pathways underlying tendon cell differentiation, through the activity of two transcription (co-)factors, EGR1 and YAP. We showed that the expression of the tendon gene SCX, the mechanosensitive gene EGR1 and YAP activity were downregulated in limb tendons of immobilized chicken fetuses. Restored muscle contraction after immobilization led to a recovery of tendon gene expression. Tendon mechanobiology was studied in vitro in fibrin- or collagen-based 3-dimensional (3D) constructs made of mesenchymal stem cells and mimicking tendon formation. Tension release in fibrin and collagen 3D-constructs induced a drop of the expression of Egr1, tendon genes and YAP activity. Overexpression of Egr1 was able to prevent the downregulation of tendon gene expression in de-tensioned fibrin 3D-constructs. YAP activity was upregulated in dynamically stretched collagen 3D-constructs and was paired with the expression of the tendon gene Scx. Chemical knock-down of YAP activity with Verteporfin (VTPF) treatment showed a decrease in the expression of YAP target genes and the tendon genes. Besides, dynamic stretch applied on VTPF-treated constructs did not restore tendon gene expression, conforting the role of YAP as an intracellular relay of mechanical cues in tendon cells. Altogether, these results highlight the importance of EGR1 and YAP downstream of mechanical forces during tendon cell differentiation
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6

Li, Jia-Wen, and 李佳玟. "Studies of p97Eps8 cellular localization in C3H10T1/2 fibroblasts." Thesis, 2003. http://ndltd.ncl.edu.tw/handle/94944396537679911955.

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碩士<br>國立成功大學<br>藥理學研究所<br>91<br>Cellular compartmentalization is important for protein functioning in cells. Eps8 (EGF receptor pathway substrate NO.8), a common substrate of EGF receptor and Src, may exist in two isoforms, i.e. 97- and 68-KDa proteins. In human tumor cell lines, constitutive tyrosine phosphorylation of Eps8 was found. Protein sequence analysis revealed the following domains of p97Eps8 that might contribute to its cellular function: a split PH domain, a putative nuclear targeting sequence (NLS), a SH3 domain, and several proline-rich regions. Our previous studies indicated that p97Eps8, but not PH-truncated p97Eps8 (i.e. 261- p97Eps8) can translocate to plasma membrane following serum stimulation in C3H10T1/2 fibroblasts. In order to further characterize the PH domain of p97Eps8 in cellular localization, we have generated Myc-tagged Eps8 and several Myc-tagged Eps8 mutant proteins including 261-p97Eps8 and the PH domain of p97Eps8 (i.e. Δ424-p97Eps8). Through biochemical and immuno-cytometric methods, we study cellular localization of the Eps8 protein. By centrifugation fractionation, we find that Δ424-p97Eps8 localize predominant in the cytosol portion (S100) of serum-treated cells. And immunofluorescent studies of theΔ424-p97Eps8 expressing cells, we find that Δ424- p97Eps8 aggregates inside the cell. We thus conclude that the PH domain alone can not translocate to plasma membrane in response to serum stimulation.
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7

Bui, Matthew. "The effect of phosphate deficiency on BMP-2 treated C3H10T1/2 mesenchymal stem cells." Thesis, 2018. https://hdl.handle.net/2144/30902.

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There are approximately 600,000 cases of delayed or aberrant fracture healing in people each year, with a small subset of these fractures experiencing disunion. Dietary phosphate deficiency has been shown to impair oxidative phosphorylation and decrease BMP-2 mediated chondrogenic differentiation during fracture healing. Prior studies using pre-committed chondro-progenitor ATDC5 cell line grown in phosphate deficient media showed that energy consumption was linked to protein production and collagen hydroxylation but inversely related to matrix mineralization. The goal of this study was to further define the relationship between energy consumption and BMP-2 mediated stem cell chondrogenic differentiation and further examine how dietary phosphate, and promotion of collagen hydroxylation via ascorbate availability effected these processes. C3H10T1/2 murine cells, a multi-potential cell line, were expanded in pre-differentiation growth medium (DMEM with 10% FBS and 1% Pen/Strep). Once cells reached 60% confluence (day 0), they were grown in differentiating media (α-MEM with 5% FBS and 1X insulin-transferrin-selenium) containing either 100% (1mM) or 25% (0.25mM) inorganic phosphate (Pi), ± 200ng/mL BMP-2(BMP), and ±0.2 mM L-ascorbic acid (AA). In total, there were 8 groups with varying combinations of these three substances. Intracellular lipid, total DNA, protein, and hydroxyproline (HP) content were examined. Chondrocyte gene expression (Col2a1, Acan, ColXa1) and adipocyte gene expression (Pparg, Plin1, Ucp1) were measured to check for cell lineage commitment and specific differentiation of the C3H10T1/2. All measurements were acquired at day 8. The +BMP differentiation media groups contained significantly less DNA content and more protein content than the –BMP differentiation media groups (both p<0.0001). There was also a significant interaction between phosphate and ascorbic acid treatment (p=0.0296), with 25% Pi +AA groups producing significantly more protein than 100% Pi +AA groups. Hydroxyproline production was not different in 100% Pi or 25% Pi conditions (p=0.2951). AA presence in culture media led to greater HP production than culture media lacking AA (p=0.0035) There was a trend of an interaction between phosphate content and AA availability (p=0.0744). 100% Pi ±AA groups produced significantly different amounts of HP while 25% Pi ±AA groups did not produce significantly different amount of HP. Col2a1, Acan, and ColXa1 expression were all increased in +BMP groups. Ascorbic acid treatment groups expressed significantly more Col2a1and Acan than –AA groups. 100% Pi media led to greater Acan expression over 25% Pi groups (p=0.0009), whereas 25% Pi media trended to lead to greater ColXa1 expression over 100% Pi groups (p=0.0734). Pparg and Plin1 expression were increased in the 25% Pi condition. There were no significant differences in expression of Ucp1. C3H10T1/2 cells were significantly affected by phosphate concentration, BMP-2 treatment, and ascorbic acid supplementation. Phosphate deficiency hindered maturation of early chondrocytes into proliferating chondrocytes while also promoting MSC differentiation into the adipocyte cell lineage. Hypertrophic chondrocyte expression was decreased in phosphate deficient media, which may coincide with increased protein production observed in low phosphate conditions. BMP-2 promoted chondrogenesis which resulted in increased protein production. Whereas, lack of ascorbic acid in cell culture media led to decreased hydroxyproline production.
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8

Chen, Yueh-Hsiang, and 陳月香. "Cloning the FOXO-overexpressed NIH3T3, 3T3-L1 and C3H10T1/2 fibroblasts." Thesis, 2010. http://ndltd.ncl.edu.tw/handle/05773638243879645066.

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碩士<br>國立中央大學<br>生命科學研究所<br>98<br>To fully understand the physiological and biochemical roles of the forkhead transcription factors FOXO1, FOXO3, FOXO4, and FOXO6 in fat cells, we stably cloned NIH3T3, 3T3-L1 and C3H10T1/2 fibroblasts with overexpression of the respective FOXO gene. Different FOXO cDNAs inserted into the pMSCV-neo vector (provided by Professor Shen-Liang Chen) were respectively transfected into murine GP+E-86 retrovirus package cells and then selected with G418 (600 μg/ml) for 2 weeks. The harvested retrovirus containing the inserted FOXO gene from the culture medium was directly transferred to NIH3T3, 3T3-L1, or C3H10T1/2 cells and G418 (600 ~ 800 μg/ml) was added to the medium 2 d after the initial infection. After an additional 2-week selection with G418, total RNA isolated from the stable clones was verified with the expression levels of FOXO gene using the methods of RT-PCR and Western blotting. We successfully cloned the NIH3T3, 3T3-L1, and C3H10T1/2 fibroblasts overexpressing with the following wild types and mutants of FOXO transcription factors: the wild types of human FOXO1 (hFOXO1-WT), mouse FoxO3 (mFoxO3-WT), mouse FoxO4 (mFoxO4-WT) , and mouse FoxO6 (mFoxO6-WT); the constitutively active mutants of human FOXO1-AAA (hFOXO1-AAA), human FOXO3-AAA (hFOXO3-AAA), human FOXO4-AAA (hFOXO4-AAA), and mouse FoxO6-S184A (mFoxO6-S184A); and a DNA binding-deficient type of human FOXO1 (hFOXO1-H215R). In NIH3T3 cells, expression with hFOXO1-WT, hFOXO1-AAA, mFoxO3-WT, hFOXO3-AAA, mFoxO6-WT, or mFoxO6-S184A reduced the cell number during a 5-day period of incubation. In 3T3-L1 preadipocytes, expression with either hFOXO1-WT、mFoxO3-WT or hFOXO3-AAA inhibited cell growth, while expression with mFOXO4-WT, or mFoxO6-WT stimulated cell growth. In C3H10T1/2 preadipocytes, expression with hFOXO1-WT, hFOXO1-AAA, hFOXO1-H215R, mFoxO4-WT, or mFoxO6-WT inhibited cell growth, while expression with either mFoxO3-WT, mFoxO4-AAA-FLAG or mFoxO6-S184A stimulated cell growth. The morphology of each clone and parental cell was observed and photographed with no significant change. Using RT-PCR, we further observed that levels of adipogenic resistin, adiponectin, and aP2 mRNAs were altered in the FOXO1-overexpressed NIH3T3, 3T3-L1 and C3H10T1/2 cells when compared to those in the empty pMSCV-neo vector-transfected cells. As NIH3T3, 3T3-L1 and C3H10T1/2 fibroblasts can be differentiated into adipocytes, results of this study suggest the different physiological and biochemical roles of the distinct FOXO transcription factors on preadipocyte growth and adipocytokine gene expression.
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9

Moseti, Dorothy. "25 Hydroxycholesterol inhibits adipogenesis and expression of adipogenic transcripts in C3H10T1/2 mouse stem cells independent of hedgehog signalling mechanism." 2015. http://hdl.handle.net/1993/30577.

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This study was conducted to assess the effects of specific oxysterols on the adipogenic differentiation and expression of adipogenic transcripts in C3H10T1/2 mouse stem cells. In the first study, four oxysterols namely; 20S, 22R, 22S and 25 hydroxycholesterol (25-HC) were tested to determine which one best inhibits adipogenesis in C3H10T1/2 mouse stem cells. Adipogenic differentiation was induced using an adipogenic media (DMITro) consisting of dexamethasone (DEX), 3-isobutyl-1-methyl-xanthine (IBMX), insulin and troglitazone (Tro). Inhibition of adipogenesis was assessed by treatment of cells with DMITro+20S, 22R, 22S or 25-HC for six days. Oil red O pictures and gene expression analysis showed that 25-HC was more effective in inhibiting the expression of adipogenic genes compared to the other oxysterols. Further investigation of the mechanisms of action of 25-HC showed that the inhibitory effects of 25-HC on adipogenesis are not mediated by hedgehog signalling.<br>October 2015
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10

Rossol-Allison, Jessica K. "Auxiliary Wnt3A Signaling in Cell Fate Decisions of C3H10T1/2 Mesenchymal Stem Cells." Diss., 2011. http://hdl.handle.net/10161/5666.

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<p>Activation of Wnt signaling pathways is critical to a variety of developmental events across all animal taxa. These highly evolutionarily conserved pathways are also important in the adult organism for maintaining homeostasis of self-renewing tissues. Because of its role in such important physiological processes, deregulation of Wnt signaling can have severe consequences; indeed, inappropriate activation of this pathway has been implicated in multiple human diseases, including cancer.</p><p>Upon binding their cellular receptors, canonical Wnt ligands, like Wnt 3A, stimulate the stabilization, accumulation, and nuclear translocation of a multifunctional cellular protein &#946;catenin, the consequence of which is induction of &#946;catenin-dependent transcription. This work describes the identification and characterization of two Wnt3A-stimulated intracellular signaling pathways activated in parallel to &#946;catenin stabilization: the RhoA pathway and the ERK pathway. These two auxiliary pathways do not affect &#946;catenin stability, accumulation, or subcellular localization; rather, they modulate &#946;catenin -dependent transcriptional activity through other mechanisms. As a result of their influence on &#946;catenin-dependent transcription, these pathways instruct cell fate decisions in C3H10T1/2 mesenchymal stem cells, in particular inhibition of adipogenesis and promotion of osteoblastogenesis.</p><p>Expression microarray analysis and biochemical and pharmacological techniques were used to further characterize the two Wnt3A-stimulated auxiliary pathways in C3H10T1/2 cells. Remarkably, each pathway influences &#946;catenin function via a novel mechanism. In the Wnt3A/RhoA pathway, Wnt3A-stimulated trimeric G proteins activate a RhoA-ROCK-SRF cascade. Activated SRF can cooperate with &#946;catenin to enhance the induction of Wnt3A target genes, like Ctgf, that also contain SRF binding sites within regulatory elements. In the Wnt3A/ERK pathway, Wnt3A transactivates the EGFR in a concentration-dependent manner, leading ultimately to ERK activation, which interacts with and promotes &#946;catenin/Tcf4 interaction and enhances induction of &#946;catenin/Tcf4 target genes. </p><p>These data emphasize the complexity of Wnt signaling and have intriguing implications regarding cross-regulation of the pathway, especially in stem cells. Also, since not all cells are capable of responding to Wnt3A by activation of these auxiliary pathways, this work identifies novel mechanisms that could underlie cell type-specific responses to Wnts and provides mechanistic insight into cellular responses to Wnt concentration gradients. Moreover, this work identifies novel transcriptional mechanisms important for promoting osteogenic cell fate specification, which could ultimately provide new therapeutic targets in disease states with bone loss or ineffective bone formation.</p><br>Dissertation
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11

Lin, Dar-Ni, and 林妲妮. "Generation and Characterization of C3H10T1/2 Fibroblasts overexpressing a membrane-associated PH-truncated 97Eps8." Thesis, 2001. http://ndltd.ncl.edu.tw/handle/52348080406725110887.

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碩士<br>國立成功大學<br>藥理學研究所<br>89<br>英文摘要(Abstract in English) Two Eps8 isoforms, p97Eps8and p68Eps8,have been identifed as common substrates for EGF receptor and Src. Previously, our laboratory observed that both tyrosyl phosphorylation and protein expression of Eps8 were elevated in v-Src transformed cells. Furthermore, overexpression of p97Eps8 potentiated serum-induced ERK activation and caused cell transformation in C3H10T1/2 fibroblasts. In contrast, cell expressing PH-truncated p97Eps8(261-p97Eps8)failed to cause cellular transformation, and enhance serum-induced ERK activation . Interestingly, unlike p97Eps8, 261-p97Eps8 was unable to localize to plasma membrane in response to serum stimulation. In order to address whether membrane association was essential for p97Eps8-mediated ERK activation and transformation, we constructed a membrane-associated 261-p97Eps8(myr-261-p97Eps8)by fusing the Src myristylation sequence (i.e. Src aa-1 to -16)to the N-terminus of 261-p97Eps8. Then, we characterized cells overexpressing myr-261-p97Eps8 and found that overexpression of myr-261-p97Eps8 in C3H10T1/2 fibroblasts caused cell transformation. And as expected, myr-261-p97Eps8 was constitutively associated with plasma membrane. Thus, we confirmed that the translocation ability of p97Eps8 conferred by infact PH domain was important for p97Eps8-induced cellular transformation.
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12

Faltin, Manuela. "Proliferation und Differenzierung der Zellkultursysteme hFOB 1.19 und C3H10T1/2 - BMP-2 unter dem Einfluss von nichtsteroidaler Antiphlogistika und einzeitiger Radiatio." Doctoral thesis, 2004. https://nbn-resolving.org/urn:nbn:de:bvb:20-opus-7854.

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Die Auswahl der Zellkulturmodelle hFOB 1.19 und C3H10T1/2 – BMP-2 erfolgte basierend auf den Hypothesen zur Entstehung heterotoper Ossifikationen. So kann die humane fetale Osteoblastenzell-Linie hFOB 1.19 in diesem Zusammenhang als determined osteoblastic progenitor cell und die murine mesenchymale Zell-Linie C3H10T1/2–BMP-2 als inducable osteoblastic progenitor cell angesehen werden. Die Zell-Linie hFOB 1.19 bietet aufgrund ihres humanen Ursprungs und der reproduzierbaren Expression osteogener Marker wie Alkalische Phosphatase, Prokollagen I und Osteocalcin die Möglichkeit, den humanen in vivo Osteogeneseprozess in vitro im Zellkultursystem zu imitieren. In der vorliegenden Studie gelingt es, im Rahmen der NSAR-Versuche die Schlüsselrolle des PGE2 sowohl im Knochenmetabolismus als auch bei der Entstehung heterotoper Ossifikationen, sowie dessen Mediatorfunktion in der Regulation osteoblastenspezifischer Differenzierungsparameter im Zellkulturmodell zu demonstrieren, obgleich der Nachweis der kalzifizierungsinhibierenden Wirkung Nichtsteroidaler Antiphlogistika, wie auch in der einschlägigen Literatur, am Zellkultursystem weiterhin aussteht. Unter Berücksichtigung aller gewonnenen Daten kann in dieser Studie dokumentiert werden, dass die murine mesenchymale Progenitorzelle C3H10T1/2 unter BMP-2-Transfizierung und der Zugabe von Ascorbat und &#61538;-Glycerophosphat zu osteoblastärer Differenzierung induziert wird, osteogene Eigenschaften entwickelt und im Längsschnitt der Studie deutliche Mineralisationstendenz aufweist<br>xxx
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13

Song, Horng-Ying, and 宋虹瑩. "Comparison of Different Frequencies of Low Intensity Pulsed Ultrasound Stimulationon C3H10T1/2 Stem Cell Growth and Differentiation." Thesis, 2011. http://ndltd.ncl.edu.tw/handle/48940022191429577773.

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碩士<br>中原大學<br>生物醫學工程研究所<br>99<br>Stem cell proliferation and differentiation play important roles on tissue regeneration. Osteogenesis of mesenchymal stem cells is the main process in bone formation. In recent years, there are more and more studies focusing on low intensity pulsed ultrasound (LIPUS) for mesenchymal stem cells differentiation, but few studies explore effects of ultrasound frequency on stem cell proliferation or differentiation. The purpose of this study is to check the frequency effects on stem cell growth. Two different single ultrasound frequency: 1 MHz (SU1) or 3 MHz (SU3) and two dynamic varying frequencies: 1 MHz stimulation following with 3 MHz (DU1/3) or 3 MHz stimulation following with 1 MHz (DU3/1) of low intensity ultrasound were used for mesenchymal stem cells treatments. Firstly, we found a proper condition for frequency response of cells on LIPUS treatment by using different percentages of fetal bovine serum (FBS) of culture medium. Secondly, proliferation and bone differentiation of stem cells were characterized by MTT, bicinchoninic acid, Alizarin red stain and alkaline phosphatase activity assay. Finally, osteogenetic gene expression (ALP, Con I, Runx2, OCN, GAPDH) of stem cells after LIPUS treatments will be investigated in detail using Polymerase Chain Reaction. The better FBS concentration of culture medium for LIPUS response evaluation on stem cell growth is 2.5%. LIPUS with varying frequencies (DU1/3) was found to enhance early differentiation of bone marrow mesenchymal stem cells significantly. The better varying frequency pattern of LIPUS for stem cell proliferation and osteogenesis differentiation has been proposed and it will be very helpful for future fracture healing acceleration in clinical.
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Faltin, Manuela [Verfasser]. "Proliferation und Differenzierung der Zellkultursysteme hFOB 1.19 und C3H10T1/2 - BMP-2 unter dem Einfluß nichtsteroidaler Antiphlogistika und einzeitiger Radiatio / vorgelegt von Manuela Faltin." 2004. http://d-nb.info/970190336/34.

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15

Cho, Young C. "Characterization of early steps in adipocyte differentiation in C3H10T1/2 cells and the inhibitory activity of the aryl hydrocarbon receptor." 2003. http://www.library.wisc.edu/databases/connect/dissertations.html.

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16

Kaps, Christian [Verfasser]. "Die Rolle von Bone-morphogenetic-Protein-Typ-I-Rezeptoren in der Bone-morphogenetic-Protein-2 abhängigen chondro- osteogenen Differenzierung der mesenchymalen Vorläuferzellinie C3H10T1/2 / von Christian Kaps." 2000. http://d-nb.info/960084479/34.

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17

Cimafranca, Melissa Antonio. "2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and epidermal growth factor (EGF) signaling inhibits in vitro adipogenesis in the mouse embryo fibroblast cell line C3H10T1/2." 2006. http://catalog.hathitrust.org/api/volumes/oclc/85783754.html.

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