Relevant bibliographies by topics / Myoblasts

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Myoblasts'

Author: Grafiati
Published: 4 June 2021
Last updated: 25 May 2024

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Consult the lists of relevant articles, books, theses, conference reports, and other scholarly sources on the topic 'Myoblasts.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Journal articles on the topic "Myoblasts"

1

Ruiz-Gómez, Mar, Nikola Coutts, Maximiliano L. Suster, Matthias Landgraf, and Michael Bate. "myoblasts incompetent encodes a zinc finger transcription factor required to specify fusion-competent myoblasts in Drosophila." Development 129, no. 1 (January 1, 2002): 133–41. http://dx.doi.org/10.1242/dev.129.1.133.

Full text
Abstract:
We report a new gene, myoblasts incompetent, essential for normal myogenesis and myoblast fusion in Drosophila. myoblasts incompetent encodes a putative zinc finger transcription factor related to vertebrate Gli proteins and to Drosophila Cubitus interruptus. myoblasts incompetent is expressed in immature somatic and visceral myoblasts. Expression is predominantly in fusion-competent myoblasts and a loss-of-function mutation in myoblasts incompetent leads to a failure in the normal differentiation of these cells and a complete lack of myoblast fusion. In the mutant embryos, founder myoblasts differentiate normally and form mononucleate muscles, but genes that are specifically expressed in fusion-competent cells are not activated and the normal downregulation of twist expression in these cells fails to occur. In addition, fusion-competent myoblasts fail to express proteins characteristic of the general pathway of myogenesis such as myosin and Dmef2. Thus myoblasts incompetent appears to function specifically in the general pathway of myogenesis to control the differentiation of fusion-competent myoblasts.
APA, Harvard, Vancouver, ISO, and other styles
2

Sun, Luguo, Kewei Ma, Haixia Wang, Fang Xiao, Yan Gao, Wei Zhang, Kepeng Wang, Xiang Gao, Nancy Ip, and Zhenguo Wu. "JAK1–STAT1–STAT3, a key pathway promoting proliferation and preventing premature differentiation of myoblasts." Journal of Cell Biology 179, no. 1 (October 1, 2007): 129–38. http://dx.doi.org/10.1083/jcb.200703184.

Full text
Abstract:
Skeletal muscle stem cell–derived myoblasts are mainly responsible for postnatal muscle growth and injury-induced muscle regeneration. However, the cellular signaling pathways controlling the proliferation and differentiation of myoblasts are not fully understood. We demonstrate that Janus kinase 1 (JAK1) is required for myoblast proliferation and that it also functions as a checkpoint to prevent myoblasts from premature differentiation. Deliberate knockdown of JAK1 in both primary and immortalized myoblasts induces precocious myogenic differentiation with a concomitant reduction in cell proliferation. This is caused, in part, by an accelerated induction of MyoD, myocyte enhancer–binding factor 2 (MEF2), p21Cip1, and p27Kip1, a faster down-regulation of Id1, and an increase in MEF2-dependent gene transcription. Downstream of JAK1, of all the signal transducer and activator of transcriptions (STATs) present in myoblasts, we find that only STAT1 knockdown promotes myogenic differentiation in both primary and immortalized myoblasts. Leukemia inhibitory factor stimulates myoblast proliferation and represses differentiation via JAK1–STAT1–STAT3. Thus, JAK1–STAT1–STAT3 constitutes a signaling pathway that promotes myoblast proliferation and prevents premature myoblast differentiation.
APA, Harvard, Vancouver, ISO, and other styles
3

McCaig, Colin D. "Myoblasts and notochord influence the orientation of somitic myoblasts from Xenopus laevis." Development 93, no. 1 (April 1, 1986): 121–31. http://dx.doi.org/10.1242/dev.93.1.121.

Full text
Abstract:
The orientation of developing myoblasts extending a bipolar axis in the presence of explanted myoblasts or whole notochord has been studied in vitro. Myoblasts tended to elongate perpendicular to the lines of diffusion of substances from these tissues. A slow-release source of agar impregnated with medium conditioned by segmented somitic myoblast or notochord also caused myoblasts to elongate perpendicular to the lines of diffusion from the source. Medium conditioned by neural tube cells or unsegmented mesoderm cells did not influence the orientation of myoblasts. It is concluded that somites and notochord release diffusible substances in vitro which are capable of directing the orientation of developing myoblasts. In vivo, a somite-derived material could play a role in determining the direction of myoblast elongation in the presomitic mesoderm. An interaction between somite and notochord-derived secretions couldinfluence the rotation of presomitic myoblasts to form a segmented somite.
APA, Harvard, Vancouver, ISO, and other styles
4

Haugk, Kathleen L., Heather-Marie P. Wilson, Karen Swisshelm, and LeBris S. Quinn. "Insulin-Like Growth Factor (IGF)-Binding Protein-Related Protein-1: An Autocrine/Paracrine Factor That Inhibits Skeletal Myoblast Differentiation but Permits Proliferation in Response to IGF1." Endocrinology 141, no. 1 (January 1, 2000): 100–110. http://dx.doi.org/10.1210/endo.141.1.7235.

Full text
Abstract:
Abstract Skeletal myogenic cells respond to the insulin-like growth factors (IGF-I and IGF-II) by differentiating or proliferating, which are mutually exclusive pathways. What determines which of these responses to IGF skeletal myoblast undergo is unclear. IGF-binding protein-related protein 1 (IGFBP-rP1) is a secreted protein with close homology to the IGF-binding proteins (IGFBPs) in the N-terminal region. IGFBP-rP1, previously called mac25 and IGFBP-7, is highly expressed in C2 skeletal myoblasts during the proliferative phase, but is down-regulated during myoblast differentiation. To determine the role of IGFBP-rP1 in myogenesis, IGFBP-rP1 was overexpressed in C2 myoblasts using a retroviral vector. Western blots indicated that the resulting C2-rP1 myoblasts secreted approximately 27-fold higher levels of IGFBP-rP1 than control C2-LX myoblasts that were transduced with a control vector (LXSN). Compared with C2-LX myoblasts, the differentiation responses of C2-rP1 myoblasts to IGF-I, IGF-II, insulin, and des(1–3)IGF-I were significantly reduced (P < 0.05). However, proliferation responses of C2-rP1 and C2-LX myoblasts to these same factors were not significantly different. Exposure of control C2-LX myoblasts to factors secreted by C2-rP1 myoblasts using a transwell coculture system reduced C2-LX myoblast differentiation significantly (P < 0.05). Experiments with the mitogen-activated protein kinase (MAPK) kinase inhibitor PD098059 suggested that IGFBP-rP1 inhibits a MAPK-dependent differentiation pathway. In confirmation of this idea, levels of phosphorylated extracellular signal-regulated kinase-2 (a MAPK) were reduced in C2-rP1 myoblasts compared with those in C2-LX myoblasts. These findings indicate that IGFBP-rP1 may function as an autocrine/paracrine factor that specifies the proliferative response to the IGFs in myogenesis.
APA, Harvard, Vancouver, ISO, and other styles
5

Fahime, E. El, M. Bouchentouf, B. F. Benabdallah, D. Skuk, J. F. Lafreniere, Y. T. Chang, and J. P. Tremblay. "Tubulyzine®, a novel tri-substituted triazine, prevents the early cell death of transplanted myogenic cells and improves transplantation success." Biochemistry and Cell Biology 81, no. 2 (April 1, 2003): 81–90. http://dx.doi.org/10.1139/o03-054.

Full text
Abstract:
Myoblast transplantation (MT) is a potential therapeutic approach for several muscular dystrophies. A major limiting factor is that only a low percentage of the transplanted myoblasts survives the procedure. Recent advances regarding how and when the myoblasts die indicate that events preceding actual tissue implantation and during the first days after the transplantation are crucial. Myoseverin, a recently identified tri-substituted purine, was shown to induce in vitro the fission of multinucleated myotubes and affect the expression of a variety of growth factors, and immunomodulation, extracellular matrix-remodeling, and stress response genes. Since the effects of myoseverin are consistent with the activation of pathways involved in wound healing and tissue regeneration, we have investigated whether pretreatment and co-injection of myoblasts with Tubulyzine® (microtubule lysing triazine), an optimized myoseverin-like molecule recently identified from a triazine library, could reduce myoblast cell death following their transplantation and consequently improves the success of myoblast transplantation. In vitro, using annexin-V labeling, we showed that Tubulyzine (5 µM) prevents normal myoblasts from apoptosis induced by staurosporine (1 µM). In vivo, the pretreatment and co-injection of immortal and normal myoblasts with Tubulyzine reduced significantly cell death (assessed by the radio-labeled thymidine of donor DNA) and increased survival of myoblasts transplanted in Tibialis anterior (TA) muscles of mdx mice, thus giving rise to more hybrid myofibers compared to transplanted untreated cells. Our results suggest that Tubulyzine can be used as an in vivo survival factor to improve the myoblast-mediated gene transfer approach.Key words: myoblast survival, mdx mouse, myoblast transplantation, microtubule-binding molecule, cell death.
APA, Harvard, Vancouver, ISO, and other styles
6

Rando, T. A., and H. M. Blau. "Primary mouse myoblast purification, characterization, and transplantation for cell-mediated gene therapy." Journal of Cell Biology 125, no. 6 (June 15, 1994): 1275–87. http://dx.doi.org/10.1083/jcb.125.6.1275.

Full text
Abstract:
The transplantation of cultured myoblasts into mature skeletal muscle is the basis for a new therapeutic approach to muscle and non-muscle diseases: myoblast-mediated gene therapy. The success of myoblast transplantation for correction of intrinsic muscle defects depends on the fusion of implanted cells with host myofibers. Previous studies in mice have been problematic because they have involved transplantation of established myogenic cell lines or primary muscle cultures. Both of these cell populations have disadvantages: myogenic cell lines are tumorigenic, and primary cultures contain a substantial percentage of non-myogenic cells which will not fuse to host fibers. Furthermore, for both cell populations, immune suppression of the host has been necessary for long-term retention of transplanted cells. To overcome these difficulties, we developed novel culture conditions that permit the purification of mouse myoblasts from primary cultures. Both enriched and clonal populations of primary myoblasts were characterized in assays of cell proliferation and differentiation. Primary myoblasts were dependent on added bFGF for growth and retained the ability to differentiate even after 30 population doublings. The fate of the pure myoblast populations after transplantation was monitored by labeling the cells with the marker enzyme beta-galactosidase (beta-gal) using retroviral mediated gene transfer. Within five days of transplantation into muscle of mature mice, primary myoblasts had fused with host muscle cells to form hybrid myofibers. To examine the immunobiology of primary myoblasts, we compared transplanted cells in syngeneic and allogeneic hosts. Even without immune suppression, the hybrid fibers persisted with continued beta-gal expression up to six months after myoblast transplantation in syngeneic hosts. In allogeneic hosts, the implanted cells were completely eliminated within three weeks. To assess tumorigenicity, primary myoblasts and myoblasts from the C2 myogenic cell line were transplanted into immunodeficient mice. Only C2 myoblasts formed tumors. The ease of isolation, growth, and transfection of primary mouse myoblasts under the conditions described here expand the opportunities to study muscle cell growth and differentiation using myoblasts from normal as well as mutant strains of mice. The properties of these cells after transplantation--the stability of resulting hybrid myofibers without immune suppression, the persistence of transgene expression, and the lack of tumorigenicity--suggest that studies of cell-mediated gene therapy using primary myoblasts can now be broadly applied to mouse models of human muscle and non-muscle diseases.
APA, Harvard, Vancouver, ISO, and other styles
7

Knudsen, K. A., L. Smith, and S. McElwee. "Involvement of cell surface phosphatidylinositol-anchored glycoproteins in cell-cell adhesion of chick embryo myoblasts." Journal of Cell Biology 109, no. 4 (October 1, 1989): 1779–86. http://dx.doi.org/10.1083/jcb.109.4.1779.

Full text
Abstract:
During myogenesis myoblasts fuse to form multinucleate cells that express muscle-specific proteins. A specific cell-cell adhesion process precedes lipid bilayer union during myoblast fusion (Knudsen, K. A., and A. F. Horwitz. 1977. Dev. Biol. 58:328-338) and is mediated by cell surface glycoproteins (Knudsen, K. A., 1985. J. Cell Biol. 101:891-897). In this paper we show that myoblast adhesion and myotube formation are inhibited by treating fusion-competent myoblasts with phosphatidylinositol-specific phospholipase C (PI-PLC). The effect of PI-PLC on myoblast adhesion is dose dependent and inhibited by D-myo-inositol 1-monophosphate and the effect on myotube formation is reversible, suggesting a specific, nontoxic effect on myogenesis by the enzyme. A soluble form of adhesion-related glycoproteins is released from fusion-competent myoblasts by treatment with PI-PLC as evidenced by (a) the ability of phospholipase C (PLC)-released material to block the adhesion-perturbing activity of a polyclonal antiserum to intact myoblasts; and (b) the ability of PLC-released glycoprotein to stimulate adhesion-perturbing antisera when injected into mice. PI-PLC treatment of fusion-competent myoblasts releases an isoform of N-CAM into the supernate, suggesting that N-CAM may participate in mediating myoblast interaction during myogenesis.
APA, Harvard, Vancouver, ISO, and other styles
8

BARNOY, Sivia, Lia SUPINO-ROSIN, and Nechama S. KOSOWER. "Regulation of calpain and calpastatin in differentiating myoblasts: mRNA levels, protein synthesis and stability." Biochemical Journal 351, no. 2 (October 10, 2000): 413–20. http://dx.doi.org/10.1042/bj3510413.

Full text
Abstract:
Calpain (Ca2+-dependent intracellular protease)-induced proteolysis has been considered to play a role in myoblast fusion to myotubes. We found previously that calpastatin (the endogenous inhibitor of calpain) diminishes transiently during myoblast differentiation. To gain information about the regulation of calpain and calpastatin in differentiating myoblasts, we evaluated the stability and synthesis of calpain and calpastatin, and measured their mRNA levels in L8 myoblasts. We show here that µ-calpain and m-calpain are stable, long-lived proteins in both dividing and differentiating L8 myoblasts. Calpain is synthesized in differentiating myoblasts, and calpain mRNA levels do not change during differentiation. In contrast, calpastatin (though also a long-lived protein in myoblasts), is less stable in differentiating myoblasts than in the dividing cells, and its synthesis is inhibited upon initiation of differentiation. Inhibition of calpastatin synthesis is followed by a diminution in calpastatin mRNA levels. A similar calpastatin mRNA diminution is observed upon drug-induced inhibition of protein translation. On the other hand, transforming growth factor β (which inhibits differentiation) allows calpastatin synthesis and prevents the diminution in calpastatin mRNA. The overall results suggest that at the onset of myoblast differentiation, calpastatin is regulated mainly at the level of translation and that an inhibition of calpastatin synthesis leads to the decrease in its mRNA stability. The existing calpastatin then diminishes, resulting in decreased calpastatin activity in the fusing myoblasts, allowing calpain activation and protein degradation required for fusion.
APA, Harvard, Vancouver, ISO, and other styles
9

Mesmer, O. T., and T. C. Lo. "Hexose transport in human myoblasts." Biochemical Journal 262, no. 1 (August 15, 1989): 15–24. http://dx.doi.org/10.1042/bj2620015.

Full text
Abstract:
The present investigation reports on the hexose transport properties of human myoblasts isolated from normal subjects and from patients with Duchenne muscular dystrophy (DMD). Similar to rat myoblast L6, normal human myoblasts possess a high- (HAHT) and a low- (LAHT) affinity hexose transport system. The non-metabolizable hexose analogue, 2-deoxyglucose, is preferentially taken up by HAHT. The transport of this analogue is the rate-limiting step in the uptake process. This human myoblast HAHT is also similar to that of the rat myoblast in its substrate specificity and in response to the energy uncouplers, cytochalasin B and phloretin. The human myoblast LAHT resembles that of rat myoblast in its insensitivity to energy uncouplers, and in its transport affinity and capacity for 3-O-methyl-D-glucose. Although DMD myoblasts resemble their normal counterpart in their ability to differentiate, they differ significantly in their hexose transport properties. In addition to HAHT and LAHT present in normal human myoblast, DMD myoblasts contain a super-high-affinity hexose transport system (SHAHT). SHAHT can be detected only at very low substrate concentrations. It differs from HAHT not only in its much higher transport affinity, but also in its response to the traditional hexose transport inhibitors. For example, SHAHT can be activated by cytochalasin B and phlorizin, whereas it is more sensitive to inhibition by phloretin. Unlike HAHT, energy uncouplers are found to be ineffective in inhibiting SHAHT. It should be mentioned that SHAHT cannot be detected in myoblasts isolated from patients with other types of myopathy. The present study serves to demonstrate that more than one hexose transport system is operating in human skeletal muscle cells, as found in other cell types.
APA, Harvard, Vancouver, ISO, and other styles
10

Fang, Qiuwen, Ming Chen, Hua-ju Li, Tena G. Goodwin, and Peter K. Law. "Vital marker for muscle nuclei in myoblast transfer." Canadian Journal of Physiology and Pharmacology 69, no. 1 (January 1, 1991): 49–52. http://dx.doi.org/10.1139/y91-008.

Full text
Abstract:
A new method is developed using Fluoro-Gold (FG) as a vital stain to label the nuclei of donor myoblasts in myoblast transfer studies. In vitro incubation with 0.01% FG for 16 h resulted in 100% nuclei labelling. Intensive fluorescence persisted following 9 days of subculture, when the human myoblasts were injected into the quadriceps of mouse recipients immunosuppressed with cyclosporine. Injected muscles showed mosaicism of host and donor nuclei 25 days after injection, indicating (i) survival and fusion among donor myoblasts, and (ii) fusion between host and donor cells. FG labelling was not observed in control muscles injected with an equal volume of FG-labelled dead myoblasts, 0.01% FG medium, or phosphate-buffered saline.Key words: Fluoro-Gold, nucleus vital stain, myoblast culture and transplant.
APA, Harvard, Vancouver, ISO, and other styles
More sources

Dissertations / Theses on the topic "Myoblasts"

1

Elia, Ines. "SNAI1 target genes in myoblasts." Doctoral thesis, Università di Siena, 2021. http://hdl.handle.net/11365/1142998.

Full text
Abstract:
SNAI proteins are zinc finger transcription factors that act as transcriptional repressors through a conserved domain (SNAG domain) located in the N-terminus of the protein. These factors bind to a palindromic sequence of the E-box group (CANNTG) in the regulatory regions of their target genes. The role of SNAI11 and SNAI2 is well known in the epithelial mesenchymal transition, where they act as regulators increasing the capacity of tumor cells to metastasize. Less is known about their role as mediators in tissue homeostasis and differentiation. Recent studies have showed SNAI1 and SNAI2 as repressors of muscle differentiation, with the function of maintaining myoblasts in an undifferentiated state during the proliferative phase. In this study, we explored the function of SNAI1 and SNAI2 in myogenesis both in vitro and in vivo. In vitro, we analyzed the expression of SNAI1 and SNAI2 in proliferating murine myoblasts, at various time points after inducing their differentiation. To evaluate their expression during myogenesis in vivo, we induced skeletal muscle regeneration by injecting the myotoxic agent Bupivacaine in the tibialis anterior muscles of wild-type and transgenic mice. We demonstrated that SNAI1 and SNAI2 are upregulated in proliferating myoblasts both in vitro and in vivo. Through the analysis of the transcriptome in C2C12 myoblasts silenced for the expression of SNAI1, we have identified several target genes, among which Fgf21 and Atf3. FGF21 is a growth factor involved in muscle differentiation as well as in glucose and lipid metabolism. In muscle differentiation, FGF21 expression is increased during myogenic differentiation and its knockdown impairs myogenic differentiation in C2C12 cells. ATF3 is a transcription factor that induces endoplasmic reticulum stress (ER-stress), phenomenon behind numerous physiological processes, including muscle differentiation and metabolism regulation. Recent studies have showed that ATF3 is able to regulate chemokine mRNA expression in C2C12 myotubes and it attenuates inflammation of skeletal muscle upon muscle-damaging eccentric exercise. Herein, we analyzed the direct involvement of SNAI1 in the regulation of Fgf21 and Atf3. For this purpose, several Fgf21 and Atf3 promoter deletion mutants, cloned in front of the reporter gene for luciferase, were generated in order to progressively exclude the possible binding sites for SNAI1. We used the Dual-Luciferase Reporter Assay System and ChIP-qPCR analysis to demonstrate that SNAI1 directly binds to the promoter region of Fgf21 and Atf3, leading to the activation of Fgf21 and Atf3 expression in mouse C2C12 myoblasts. Finally, we generated a SNAI1 knockout C2C12 cell line, using the CRISPR-Cas9 genome editing technique and we confirmed that SNAI1 acts as repressor of Fgf21 and Atf3 in proliferating myoblasts.
APA, Harvard, Vancouver, ISO, and other styles
2

Mahabir, Mark Ashford. "Senescence in normal and DMD myoblasts." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2001. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/MQ58835.pdf.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Zhao, Shuai. "Effects of Hypoxic Conditions on Skeletal Myoblasts." Cleveland State University / OhioLINK, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=csu1482831468411105.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Babić, Nikolina. "Regulation of energy metabolism of heart myoblasts /." Thesis, Connect to this title online; UW restricted, 2004. http://hdl.handle.net/1773/11563.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Yazid, Muhammad Da'In Bin. "Analysis of cell signalling in dystrophin-deficient myoblasts." Thesis, University of Birmingham, 2017. http://etheses.bham.ac.uk//id/eprint/7342/.

Full text
Abstract:
An absence of dystrophin in muscle has a massive impact throughout muscle development, and Duchene Muscular Dystrophy (DMD) is one of the consequences. The disruption of the dystrophin-glycoprotein complex (DGC) is caused by a mutation in the dmd gene, which effects muscle integrity, resulting in progressive muscle degeneration and weakness. In this study, dfd13 (dystrophin-deficient) and C2C12 (non-dystrophic) myoblasts were cultured in low mitogen conditions for 10 days to induce differentiation; however, dfdl3 myoblasts did not achieve terminal differentiation. It has been suggested that Pax7 may play a major role during myogenesis, therefore its expression pattern and transport protein were examined for any impairments. It was established that Pax7 localises in the cytoplasm of dystrophindeficient myoblasts and high expression is retained during differentiation. Colocalisation of Pax7 with subcellular markers analysis indicated that Pax7 is synthesised during the proliferative state. Pax7 was shown to possess a nuclear location signal and KPNA2 was suggested as escort protein for Pax7 translocation into the nucleus. The PTEN-PI3K/Akt signalling pathway was investigated and protein synthesis regulation and Fox03 was found to be impaired. Autophagy related genes were found to be highly expressed; however, LC3 lipidation and autophagy flux showed a reduction upon differentiation, indicating defective autophagy. The contribution of PTEN overexpression was assessed in relation to endoplasmic reticulum (ER) stress and activation of the unfolding protein response (UPR). It was established that a reduction in ER stress and changes to UPR activation lead to apoptosis. Finally, minidystrophintransfection of both types of myoblasts was utilised to examine the effect, especially in dystrophin-deficient myoblasts. Minidystrophin improved protein synthesis activation and increased autophagy (increased LC3 lipidation), suggesting that minidystrophin ameliorates dystrophic events at the level of autophagosome formation. To conclude, destabilisation of the plasma membrane owing to a dystrophin mutation causes cell signalling alterations which minidystrophin restoration can partly improve.
APA, Harvard, Vancouver, ISO, and other styles
6

Akohene-Mensah, Paul. "Examining the Role of L-Type Amino Acid Transporter 1 (SLC7A5) in Myoblasts." Thesis, Université d'Ottawa / University of Ottawa, 2020. http://hdl.handle.net/10393/41036.

Full text
Abstract:
Skeletal muscles represent the largest tissue mass within the body and are primarily involved in the generation of force for voluntary movement. Skeletal muscles have a remarkable capacity to repair, due primarily to the actions of muscle stem cells (MuSCs). MuSCs are normally quiescent in adult skeletal muscle; however, in response to myotrauma (trauma to muscle tissue) from muscle injury or exercise, MuSCs become activated, either undergo self-renewal to replenish the quiescent population or commit to the myogenic lineage as myoblasts, proliferate, and differentiate into myotubes in vitro or fuse to existing myofibers in vivo. This process of generating new myofibers from quiescent MuSCs is termed myogenesis and a full understanding of how myogenesis is regulated remains to be understood. Mounting evidence suggests that amino acids, particularly the essential amino acid leucine, play a role in MuSC regulation. Leucine is specifically translocated and sensed by the L-type amino acid transporter 1 (LAT1); which facilitates leucine uptake in mature myofibers. Inside the cell, leucine activates mammalian or mechanistic target of rapamycin complex 1 (mTORC1) to stimulate cell growth, proliferation, and protein synthesis. Whether leucine has direct effects on myoblast function via LAT1 is unknown. Thus, our overall objective was to begin to characterize the role of LAT1 in myogenesis. Our results indicate that myoblasts differentially expressed LAT1 throughout myogenesis with peak protein content occurring during differentiation (p<0.05 vs. early proliferation). Further, our results indicate thatpharmacological LAT1 inhibition reduced myoblast expansion and differentiation in vitro (both p<0.05 vs. control). Interestingly, myoblast LAT1 protein content did not change in response to leucine supplementation in vitro; however, was lower under in vitro atrophic conditions (p<0.05 vs. control). Based on these findings, we conclude that LAT1 plays an important role in regulating myogenesis. As such, we uncover a novel role for LAT1 in regulating muscle mass via contributing to the control of MuSC function.
APA, Harvard, Vancouver, ISO, and other styles
7

Gersbach, Charles Alan. "Runx2-Genetically Engineered Skeletal Myoblasts for Bone Tissue Engineering." Diss., Georgia Institute of Technology, 2006. http://hdl.handle.net/1853/11600.

Full text
Abstract:
Bone tissue engineering is a promising approach to address the limitations of currently used bone tissue substitutes. However, an optimal cell source for the production of osteoblastic matrix proteins and mineral deposition has yet to be defined. In response to this deficiency, ex vivo gene therapy of easily accessible non-osteogenic cells, such as skeletal myoblasts, has become a prevalent strategy for inducing an osteoblastic phenotype. The majority of these approaches focus on constitutive overexpression of soluble osteogenic growth factors such as bone morphogenetic proteins (BMPs). In order to avoid aberrant effects of unregulated growth factor secretion, this work focuses on delivery of the osteoblastic transcription factor Runx2 as an autocrine osteogenic signal under the control of an inducible expression system. The overall objective of this research was to engineer an inducible cell source for bone tissue engineering that addresses the limitations of current cell-based approaches to orthopedic regeneration. Our central hypothesis was that inducible Runx2 overexpression in skeletal myoblasts would stimulate differentiation into a regulated osteoblastic phenotype. We have demonstrated that Runx2 overexpression stimulates transdifferentiation of primary skeletal myoblasts into a mineralizing osteoblastic phenotype. Furthermore, we have established Runx2-engineered skeletal myoblasts as a potent cell source for bone tissue engineering applications in vitro and in vivo, similar to BMP-2-overexpressing controls. Finally, we exogenously regulated osteoblastic differentiation by myoblasts engineered to express a tetracycline-inducible Runx2 transgene. This conversion into an osteoblastic phenotype was inducible, repressible, recoverable after suppression, and dose-dependent with tetracycline concentration. This work is significant because it addresses cell sourcing limitations of bone tissue engineering, develops controlled and effective gene therapy methods for orthopedic regeneration, and establishes a novel strategy for regulating the magnitude and kinetics of osteoblastic differentiation.
APA, Harvard, Vancouver, ISO, and other styles
8

Mazzuca, Delfina Maria. "Regulation and function of glucose transporters in rat myoblasts." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp01/MQ30668.pdf.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Ren, Huiping. "MBD2bdemethylase is involved in the myogenesis of C2C12 myoblasts." Thesis, McGill University, 2003. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=80861.

Full text
Abstract:
Initiating the muscle differentiation pathway typically results in activation of muscle-specific genes previously maintained in a silenced state. One of the processes controlling changes in gene expression during differentiation is a global demethylation event. The mechanisms involved in this global hypomethylation are not fully understood.
Promoter methylation is one of the normal mechanisms inactivating gene expression. A single CpG site in the 5' flanking region of myogenin is reported to undergo demethylation during C2C12 differentiation. Considering the demethylase feature of MBD2b and its expression profile during C2C12 differentiation, I propose the hypothesis that MBD2b/demethylase is involved in C2C12 differentiation by demethylating the promoter of the myogenin gene as well as other genes involved in myogenic differentiation.
To test this hypothesis, I determined the consequences of up-regulation and down-regulation of MBD2b/demethylase in C2C12 cells.
The state of the myogenin promoter was also altered as determined using a probe recognizing a single HpaII site, which was previously reported to become demethylated during C2C12 differentiation. (Abstract shortened by UMI.)
APA, Harvard, Vancouver, ISO, and other styles
10

Lund, Dane. "It's a Jungle Out There| Myoblasts, Matrix, and MMPs." Thesis, University of Missouri - Columbia, 2016. http://pqdtopen.proquest.com/#viewpdf?dispub=10182609.

Full text
APA, Harvard, Vancouver, ISO, and other styles
More sources

Books on the topic "Myoblasts"

1

Mahabir, Mark Ashford. Senescence in normal and DMD myoblasts. Ottawa: National Library of Canada, 2001.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
2

International Conference on Myoblast Transfer Therapy (1989 New York, N.Y.). Myoblast transfer therapy. New York: Plenum Press, 1990.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
3

Miller, Mathew Gordon. Integrin-Linked Kinase 1 (ILK1) is necessary for myogenic differentiation in rat L6 myoblasts. Ottawa: National Library of Canada, 2000.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
4

Griggs, Robert C., and George Karpati, eds. Myoblast Transfer Therapy. Boston, MA: Springer US, 1990. http://dx.doi.org/10.1007/978-1-4684-5865-7.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Muscular Dystrophy Association International Conference on Myoblast Transfer Therapy (1989 New York, N.Y.). Myoblast transfer therapy. New York: Plenum Press, 1990.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
6

Myoblast transfer: Gene therapy for muscular dystrophy. Austin: R.G. Landes, 1994.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
7

Zeytinoğlu, Hülya. Effects of the N-ras oncogene on differentiation of CO25 myoblast cells. Norwich: University of EastAnglia, 1992.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
8

Wong, Karen. Expression of myostatin during insulin-like growth factor-I-induced myoblast proliferation and differentiation. Ottawa: National Library of Canada, 2002.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
9

1957-, Metzger Joseph Mark, ed. Cardiac cell and gene transfer: Principles, protocols, and applications. Totowa, N.J: Humana Press, 2003.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
10

Media, Springer Science+Business, ed. Cellular cardiomyoplasty: Methods and protocols. New York: Humana Press, 2013.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
More sources

Book chapters on the topic "Myoblasts"

1

Stockdale, Frank E., E. Janet Hager, Susan E. Fernyak, and Joseph X. DiMario. "Myoblasts, Satellite Cells, and Myoblast Transfer." In Myoblast Transfer Therapy, 7–11. Boston, MA: Springer US, 1990. http://dx.doi.org/10.1007/978-1-4684-5865-7_2.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Rao, Vinay Kumar, Shilpa Rani Shankar, and Reshma Taneja. "Chromatin Immunoprecipitation in Skeletal Myoblasts." In Methods in Molecular Biology, 43–54. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-8897-6_4.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Grounds, Miranda D. "The Proliferation and Fusion of Myoblasts In Vivo." In Myoblast Transfer Therapy, 101–6. Boston, MA: Springer US, 1990. http://dx.doi.org/10.1007/978-1-4684-5865-7_13.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Schwartz, Lawrence M., Zhengliang Gao, Christine Brown, Sangram S. Parelkar, and Honor Glenn. "Cell Death in Myoblasts and Muscles." In Methods in Molecular Biology, 313–32. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60327-017-5_22.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Schopf, Gerhard, Helmut Rumpold, and Mathias M. Müller. "Purine Salvage in Rat Heart Myoblasts." In Purine and Pyrimidine Metabolism in Man V, 511–15. New York, NY: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4684-1248-2_79.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Ismail, Nahed, Gonzalo Hortelano, and Ayman Al-Hendy. "Growth Hormone Gene Therapy Using Encapsulated Myoblasts." In Cell Encapsulation Technology and Therapeutics, 343–50. Boston, MA: Birkhäuser Boston, 1999. http://dx.doi.org/10.1007/978-1-4612-1586-8_27.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Lapan, Ariya D., and Emanuela Gussoni. "Isolation and Characterization of Human Fetal Myoblasts." In Methods in Molecular Biology, 3–19. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-343-1_1.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Blau, Helen M., Cecelia Webster, and Grace K. Pavlath. "Purification and Proliferation of Human Myoblasts Isolated with Fluorescence Activated Cell Sorting." In Myoblast Transfer Therapy, 97–100. Boston, MA: Springer US, 1990. http://dx.doi.org/10.1007/978-1-4684-5865-7_12.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Moreno, Nerea, Irene González-Martínez, Rubén Artero, and Estefanía Cerro-Herreros. "Rapid Determination of MBNL1 Protein Levels by Quantitative Dot Blot for the Evaluation of Antisense Oligonucleotides in Myotonic Dystrophy Myoblasts." In Methods in Molecular Biology, 207–15. New York, NY: Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-2010-6_13.

Full text
Abstract:
AbstractWestern blot assays are not adequate for high-throughput screening of protein expression because it is an expensive and time-consuming technique. Here we demonstrate that quantitative dot blots in plate format are a better option to determine the absolute contents of a given protein in less than 48 h. The method was optimized for the detection of the Muscleblind-like 1 protein in patient-derived myoblasts treated with a collection of more than 100 experimental oligonucleotides.
APA, Harvard, Vancouver, ISO, and other styles
10

Rosengart, Todd K., and B. S. Muath Bishawi. "Regenerating Mechanical Function In Vivo with Skeletal Myoblasts." In Regenerating the Heart, 201–17. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-021-8_12.

Full text
APA, Harvard, Vancouver, ISO, and other styles

Conference papers on the topic "Myoblasts"

1

Calve, Sarah, and Hans-Georg Simon. "The Mechanical and Biochemical Environment Controls Cellular Differentiation During Muscle Regeneration." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53767.

Full text
Abstract:
Urodele amphibians like the newt, are able to completely regenerate lost organs and appendages without scarring. Differentiated tissues are considered a reservoir for uncommitted blastema cells that participate in the regeneration of the lost structure. To determine the influence of the extracellular matrix (ECM) on the recruitment of progenitor cells from the skeletal muscle, we immunohistochemically mapped the limb in 3D and found that a transitional ECM rich in hyaluronic acid (HA), tenascin-C (TN) and fibronectin (FN) is dynamically expressed during the early stages of regeneration [1]. Functional in vitro testing of different ECM components on primary muscle cells revealed that HA and TN support myoblast migration, inhibit differentiation and enhance the fragmentation of multinucleate myotubes and production of viable mononucleate myoblasts, cellular behaviors necessary for blastema formation [1]. In contrast, myoblasts plated on matrices that mimic ECM around differentiated muscle (FN, Matrigel and laminin) induced both proliferation and fusion.
APA, Harvard, Vancouver, ISO, and other styles
2

Hashimoto, Shigehiro. "Hysteresis Effect of Tangential Force Field With Centrifuge on Myoblast: Cultured on Striped Pattern of Micro Ridge for Direction Control." In ASME 2021 Fluids Engineering Division Summer Meeting. American Society of Mechanical Engineers, 2021. http://dx.doi.org/10.1115/fedsm2021-65639.

Full text
Abstract:
Abstract Hysteresis effects of the direction of mechanical stimulation on the cell behavior have been examined in vitro. A micro ridge pattern was made on the surface of the scaffold to align the directions of the cells being stimulated. The stripe pattern (0.7 μm heigh, 3 μm wide, and 3 μm interval) was created by the photolithography technique. Three regions, which have the uniform value of the angle between the longitudinal direction of the ridge and the direction of the tangential force, were set: 0, 45, and 90 degrees in each region. Myoblasts (C2C12: mouse myoblast cell line) were used in the experiment. The scaffold plate with cells was set in the tube of a conventional centrifuge placed in an incubator to apply the tangential force field to each cell. After the cell culture for 5 hours with centrifugation, the behavior of each cell was analyzed on time-lapse microscopic images for 10 hours. Experimental results show that cell activities (migration and deformation) are enhanced after stimulation of tangential forces perpendicular to the long axis of myoblasts.
APA, Harvard, Vancouver, ISO, and other styles
3

Yonezawa, Hiroki, Shigehiro Hashimoto, and Haruki Kinoshiro. "Behavior of Myoblasts in Confluent Layer Under Shear Flow Field." In ASME 2022 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2022. http://dx.doi.org/10.1115/imece2022-96619.

Full text
Abstract:
Abstract To investigate the effect of shear stress direction on cell orientation, the movement of each cell parallel or perpendicular to the direction of the shear flow field in the two-dimensional confluent layer was investigated in vitro. A Couette-type shear flow between parallel walls was formed between the lower static culture disc and the upper rotating disc. Shear stress (1 Pa) was set by adjusting the rotation speed of the upper disk. After culturing to confluence in a flowless state to adhere myoblasts (C2C12: mouse myoblast line) to the lower disk, shear flow was continuously applied for 7 days in an incubator (incorporated with an inverted phase contrast microscope). The migration of each cell was tracked in the time-lapse images. Experiments have shown that cells migrate along the long axis (not only parallel, but also vertical to the shear stress). This method can be applied to maintain the orientation of muscle cells in the engineered tissue.
APA, Harvard, Vancouver, ISO, and other styles
4

Koppes, Ryan A., Nathan R. Schiele, Douglas M. Swank, Douglas B. Chrisey, and David T. Corr. "Passive Mechanical Analysis of Engineered Myotube Fibers." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-206825.

Full text
Abstract:
The loss of functional muscle as a product of genetic disease, traumatic injury, or surgical excisions results in a physiological deficiency that still remains without an effective clinical treatment [1]. Engineering of functional tissue in vitro for replacement in vivo might pose as a potential remedy for this clinical demand. By approaching tissue engineering from the bottom-up, geometrically directing myoblast growth provides a means for constructing tissue replacements cell-by-cell versus the traditional decellularized construct that remains limited by its size and ability to deliver cellular nutrients. Furthermore, geometrically controlling the growth of myoblasts allows for direct manipulation of the structural and mechanical properties inherent to muscular tissue.
APA, Harvard, Vancouver, ISO, and other styles
5

Guirguis, Mark, Katelyn Rimkunas, Michael Raymond, and Leo Q. Wan. "Cell Organelle Positioning of Micropatterned Single C2C12 Mouse Myoblasts." In 2013 39th Annual Northeast Bioengineering Conference (NEBEC). IEEE, 2013. http://dx.doi.org/10.1109/nebec.2013.168.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Basualto-Alarcόn, C., MF Bozán, J. Bevilacqua, F. Urra, D. González, H. Gatica, A. Göecke, et al. "AB0176 Mitochondrial dysfunction in idiopathic inflammatory myopathy derived myoblasts." In Annual European Congress of Rheumatology, 14–17 June, 2017. BMJ Publishing Group Ltd and European League Against Rheumatism, 2017. http://dx.doi.org/10.1136/annrheumdis-2017-eular.3889.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Hashimoto, Shigehiro, and Hiroki Yonezawa. "Tracings of Behavior of Myoblasts Cultured Under Couette Type of Shear Flow Between Parallel Disks." In ASME 2021 Fluids Engineering Division Summer Meeting. American Society of Mechanical Engineers, 2021. http://dx.doi.org/10.1115/fedsm2021-65207.

Full text
Abstract:
Abstract A cell deforms and migrates on the scaffold under mechanical stimuli in vivo. In this study, a cell with division during shear stress stimulation has been observed in vitro. Before and after division, both migration and deformation of each cell were analyzed. To make a Couette-type shear flow, the medium was sandwiched between parallel disks (the lower stationary culture-disc and the upper rotating disk) with a constant gap. The wall shear stress (1.5 Pa &lt; τ &lt; 2 Pa) on the surface of the lower culture plate was controlled by the rotational speed of the upper disc. Myoblasts (C2C12: mouse myoblast cell line) were used in the test. After cultivation without flow for 24 hours for adhesion of the cells to the lower disk, constant τ was applied to the cells in the incubator for 7 days. The behavior of each cell during shear was tracked by time-lapse images observed by an inverted phase contrast microscope placed in the incubator. Experimental results show that each cell tends to divide after higher activities: deformation and migration. The tendency is remarkable at the shear stress of 1.5 Pa.
APA, Harvard, Vancouver, ISO, and other styles
8

Hashimoto, Shigehiro, and Shogo Uehara. "Cell Behavior in Flow Passing Through Micro Machined Gap." In ASME 2021 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2021. http://dx.doi.org/10.1115/imece2021-69690.

Full text
Abstract:
Abstract Does each cell show specified behavior (deformation and alignment) as it passes through the micro-gap in the flow channel? A gap with a rectangular cross section (10 μm high, 0.4 mm wide, and length 0.1 mm long) was manufactured in the middle part of the flow path by photolithography technique. Myoblasts (C2C12: mouse myoblast cell line) sparsely suspended in the medium were used for the test. Deformation of each cell passing through the micro-gap was observed with an inverted phase contrast microscope. From the contour of the image of each cell passing through the gap, several parameters were analyzed: the two-dimensional projected area, the degree of deformation by ellipse approximation, and the alignment of the major axis of the deformed cell. The experimental results show that the alignment of each cell tends to deviate from the flow direction as the larger projected two-dimensional area.
APA, Harvard, Vancouver, ISO, and other styles
9

Hashimoto, Shigehiro, Kiyoshi Yoshinaka, and Hiroki Yonezawa. "Behavior of Cell Passing Through Micro Slit Between Micro Machined Plates." In ASME 2021 Fluids Engineering Division Summer Meeting. American Society of Mechanical Engineers, 2021. http://dx.doi.org/10.1115/fedsm2021-65209.

Full text
Abstract:
Abstract Deformation of each cell, as it passes through the micro-slit in the flow channel, has been investigated in vitro. A slit with a rectangular cross section (height 10 μm, width 0.4 mm, length 0.1 mm) was made in the center of the flow path by photolithography technique. Myoblasts (C2C12: mouse myoblast cell line) were used for the test. The flow rate of the medium, in which the cells were suspended, was controlled by a pressure head between the inlet and the outlet. Deformation of each cell passing through the micro-slit was observed with an inverted phase contrast microscope. Using the contour of the image of each cell passing through the slit intermittently, several parameters were analyzed: the two-dimensional projected area, the degree of deformation by ellipse approximation, and the deformation direction. The experimental results show that elongation of the cell in the slit tends to decrease the area of the cell.
APA, Harvard, Vancouver, ISO, and other styles
10

Hashimoto, Shigehiro, and Takashi Yokomizo. "Tracings of Interaction Between Myoblasts Under Shear Flow in Vitro." In ASME 2021 Fluids Engineering Division Summer Meeting. American Society of Mechanical Engineers, 2021. http://dx.doi.org/10.1115/fedsm2021-65203.

Full text
Abstract:
Abstract How does the group of cells make orientation perpendicular to the flow direction? How does contact with an adjacent cell affect the orientation of the cell? The orientation of a cell according to the neighbor cell under shear flow fields has been traced in vitro. A Couette type flow device with parallel discs was manufactured for the cell culture under the controlled constant wall shear stress. Cells (C2C12: mouse myoblast cell line) were cultured on the lower disc while applying the shear flow in the medium by the upper rotating disc. After culture for 24 hours without flow for adhesion of cells, 2 Pa of the constant wall shear stress was continuously applied in the incubator for 7 days. The behavior of each cell was traced by time-lapse images observed by an inverted phase contrast microscope placed in an incubator. The experiment shows the following results quantitatively by parameters: the contact ratio, and the angle between major axes of cells approximated to ellipsoids. As the ratio of the contact length with the adjacent cell to the pericellular length increases in the two-dimensional projection images, the adjacent cells tend to be oriented in parallel with each other.
APA, Harvard, Vancouver, ISO, and other styles

Reports on the topic "Myoblasts"

1

Halevy, Orna, Zipora Yablonka-Reuveni, and Israel Rozenboim. Enhancement of meat production by monochromatic light stimuli during embryogenesis: effect on muscle development and post-hatch growth. United States Department of Agriculture, June 2004. http://dx.doi.org/10.32747/2004.7586471.bard.

Full text
Abstract:
The original objectives were: A. To determine the critical embryonic age for monochromatic green light stimulation. B. To follow the ontogeny of embryos exposed to monochromatic green light vs. darkness. C. To investigate the effects of monochromatic green light illumination on myoblast and fiber development in the embryo. D. To investigate the stimulatory effect of light combinations during embryo and post-hatch periods on growth and meat production. E. To evaluate the direct effect of monochromatic green light on cultured embryonic and adult myoblasts. The overall purpose of this study was to investigate the effect of monochromatic light stimuli during incubation period of broilers on muscle development and satellite cell myogenesis. Based on previous studies (Halevy et al., 1998; Rozenboim et al., 1999) that demonstrated the positive effects of green-light illumination on body and muscle growth, we hypothesized that monochromatic light illumination accelerates embryo and muscle development and subsequently enhances muscle growth and meat production. Thus, further decreases management costs. Under the cooperation of the laboratories at the Hebrew University of Jerusalem and University of Washington we have conducted the following: 1. We have established the critical stage for exposure to green monochromatic light which has the maximal effect on body and muscle growth (Objective A). We report that embryonic day 5 is optimal for starting illumination. The optimal regime of lighting that will eliminate possible heat effects was evaluated by monitoring egg core temperature at various illumination periods. We found that intermitted lighting (15 min. on; 15 min. off) is optimal to avoid heat effects. 2. We have evaluated in detail gross changes in embryo development profile associated to green light stimuli vs. darkness. In addition, we have investigated the stimulatory effect of light combinations during embryo and post-hatch periods on body and muscle growth (Objective B,D). 3. We have studied the expression profile of muscle regulatory proteins during chicken muscle cell differentiation in cultures using newly developed antibodies. This study paved the way for analyzing the expression of these proteins in our photo stimulation experiments (Objective C). 4. We have studied the pattern ofPax7 expression during myogenesis in the posthatch chicken. Experimental chick pectoralis muscles as well adult myoblast cultures were used in this study and the results led us to propose a novel model for satellite cell differentiation and renewal. 5. The effects of monochromatic green light illumination during embryogenesis have been studied. These studies focused on fetal myoblast and satellite cell proliferation and differentiation at pre- and posthatch periods and on the effects on the expression of muscle regulatory proteins which are involved in these processes. In addition, we have analyzed the effect of photo stimulation in the embryo on myofiber development at early posthatch (Objective C). 6. In follow the reviewers' comments we have not conducted Objective E. The information gathered from these studies is of utmost importance both, for understanding the molecular basis of muscle development in the posthatch chicks and for applied approach for future broiler management. Therefore, the information could be beneficial to agriculture in the short term on the one hand and to future studies on chick muscle development in the embryo and posthatch on the other hand.
APA, Harvard, Vancouver, ISO, and other styles
2

Shani, Moshe, and C. P. Emerson. Genetic Manipulation of the Adipose Tissue via Transgenesis. United States Department of Agriculture, April 1995. http://dx.doi.org/10.32747/1995.7604929.bard.

Full text
Abstract:
The long term goal of this study was to reduce caloric and fat content of beef and other red meats by means of genetic modification of the animal such that fat would not be accumulated. This was attempted by introducing into the germ line myogenic regulatory genes that would convert fat tissue to skeletal muscle. We first determined the consequences of ectopic expression of the myogenic regulatory gene MyoD1. It was found that deregulation of MyoD1 did not result in ectopic skeletal muscle formation but rather led to embryonic lethalities, probably due to its role in the control of the cell cycle. This indicated that MyoD1 should be placed under stringent control to allow survival. Embryonic lethalities were also observed when the regulatory elements of the adipose-specific gene adipsin directed the expression of MyoD1 or myogenin cDNAs, suggesting that these sequences are probably not strong enough to confer tissue specificity. To determine the specificity of the control elements of another fat specific gene (adipocyte protein 2-aP2), we fused them to the bacterial b-galactosidase reporter gene and established stable transgenic strains. The expression of the reporter gene in none of the strains was adipose specific. Each strain displayed a unique pattern of expression in various cell lineages. Most exciting results were obtained in a transgenic strain in which cells migrating from the ventro-lateral edge of the dermomyotome of developing somites to populate the limb buds with myoblasts were specifically stained for lacZ. Since the control sequences of the adipsin or aP2 genes did not confer fat specificity in transgenic mice we have taken both molecular and genetic approaches as an initial effort to identify genes important in the conversion of a multipotential cell such as C3H10T1/2 cell to adipoblast. Several novel adipocyte cell lines have been established that differ in the expression of transcription factors of the C/EBP family known to be markers for adipocyte differentiation. These studies revealed that one of the genetic programming changes which occur during 10T1/2 conversion from multipotential cell to a committed adipoblast is the ability to linduce C/EBPa gene expression. It is expected that further analysis of this gene would identify elements which regulate this lineage-specific expression. Such elements might be good candidates in future attempts to convert adipoblasts to skeletal muscle cells in vivo.
APA, Harvard, Vancouver, ISO, and other styles
3

Halevy, Orna, Sandra Velleman, and Shlomo Yahav. Early post-hatch thermal stress effects on broiler muscle development and performance. United States Department of Agriculture, January 2013. http://dx.doi.org/10.32747/2013.7597933.bard.

Full text
Abstract:
In broilers, the immediate post-hatch handling period exposes chicks to cold or hot thermal stress, with potentially harmful consequences to product quantity and quality that could threaten poultry meat marketability as a healthy, low-fat food. This lower performance includes adverse effects on muscle growth and damage to muscle structure (e.g., less protein and more fat deposition). A leading candidate for mediating the effects of thermal stress on muscle growth and development is a unique group of skeletal muscle cells known as adult myoblasts (satellite cells). Satellite cells are multipotential stem cells that can be stimulated to follow other developmental pathways, especially adipogenesis in lieu of muscle formation. They are most active during the first week of age in broilers and have been shown to be sensitive to environmental conditions and nutritional status. The hypothesis of the present study was that immediate post-hatch thermal stress would harm broiler growth and performance. In particular, growth characteristics and gene expression of muscle progenitor cells (i.e., satellite cells) will be affected, leading to increased fat deposition, resulting in long-term changes in muscle structure and a reduction in meat yield. The in vitro studies on cultured satellite cells derived from different muscle, have demonstrated that, anaerobic pectoralis major satellite cells are more predisposed to adipogenic conversion and more sensitive during myogenic proliferation and differentiation than aerobic biceps femoris cells when challenged to both hot and cold thermal stress. These results corroborated the in vivo studies, establishing that chronic heat exposure of broiler chicks at their first two week of life leads to impaired myogenicity of the satellite cells, and increased fat deposition in the muscle. Moreover, chronic exposure of chicks to inaccurate temperature, in particular to heat vs. cold, during their early posthatch periods has long-term effects of BW, absolute muscle growth and muscle morphology and meat quality. The latter is manifested by higher lipid and collagen deposition and may lead to the white striping occurrence. The results of this study emphasize the high sensitivity of muscle progenitor cells in the early posthatch period at a time when they are highly active and therefore the importance of rearing broiler chicks under accurate ambient temperatures. From an agricultural point of view, this research clearly demonstrates the immediate and long-term adverse effects on broiler muscling and fat formation due to chronic exposure to hot stress vs. cold temperatures at early age posthatch. These findings will aid in developing management strategies to improve broiler performance in Israel and the USA. BARD Report - Project4592 Page 2 of 29
APA, Harvard, Vancouver, ISO, and other styles
4

Yahav, Shlomo, John Brake, and Orna Halevy. Pre-natal Epigenetic Adaptation to Improve Thermotolerance Acquisition and Performance of Fast-growing Meat-type Chickens. United States Department of Agriculture, September 2009. http://dx.doi.org/10.32747/2009.7592120.bard.

Full text
Abstract:
: The necessity to improve broiler thermotolerance and performance led to the following hypothesis: (a) thethermoregulatory-response threshold for heat production can be altered by thermal manipulation (TM) during incubation so as to improve the acquisition of thermotolerance in the post-hatch broiler;and (b) TM during embryogenesis will improve myoblast proliferation during the embryonic and post-hatch periods with subsequent enhanced muscle growth and meat production. The original objectives of this study were as follow: 1. to assess the timing, temperature, duration, and turning frequency required for optimal TM during embryogenesis; 2. to evaluate the effect of TM during embryogenesis on thermoregulation (heat production and heat dissipation) during four phases: (1) embryogenesis, (2) at hatch, (3) during growth, and (4) during heat challenge near marketing age; 3. to investigate the stimulatory effect of thermotolerance on hormones that regulate thermogenesis and stress (T₄, T₃, corticosterone, glucagon); 4. to determine the effect of TM on performance (BW gain, feed intake, feed efficiency, carcass yield, breast muscle yield) of broiler chickens; and 5. to study the effect of TM during embryogenesis on skeletal muscle growth, including myoblast proliferation and fiber development, in the embryo and post-hatch chicks.This study has achieved all the original objectives. Only the plasma glucagon concentration (objective 3) was not measured as a result of technical obstacles. Background to the topic: Rapid growth rate has presented broiler chickens with seriousdifficulties when called upon to efficiently thermoregulate in hot environmental conditions. Being homeotherms, birds are able to maintain their body temperature (Tb) within a narrow range. An increase in Tb above the regulated range, as a result of exposure to environmental conditions and/or excessive metabolic heat production that often characterize broiler chickens, may lead to a potentially lethal cascade of irreversible thermoregulatory events. Exposure to temperature fluctuations during the perinatal period has been shown to lead to epigenetic temperature adaptation. The mechanism for this adaptation was based on the assumption that environmental factors, especially ambient temperature, have a strong influence on the determination of the “set-point” for physiological control systems during “critical developmental phases.” In order to sustain or even improve broiler performance, TM during the period of embryogenesis when satellite cell population normally expand should increase absolute pectoralis muscle weight in broilers post-hatch. Major conclusions: Intermittent TM (39.5°C for 12 h/day) during embryogenesis when the thyroid and adrenal axis was developing and maturing (E7 to E16 inclusive) had a long lasting thermoregulatory effect that improved thermotolerance of broiler chickens exposed to acute thermal stress at market age by lowering their functional Tb set point, thus lowering metabolic rate at hatch, improving sensible heat loss, and significantly decreasing the level of stress. Increased machine ventilation rate was required during TM so as to supply the oxygen required for the periods of increased embryonic development. Enhancing embryonic development was found to be accomplished by a combination of pre-incubation heating of embryos for 12 h at 30°C, followed by increasing incubation temperature to 38°C during the first 3 days of incubation. It was further facilitated by increasing turning frequency of the eggs to 48 or 96 times daily. TM during critical phases of muscle development in the late-term chick embryo (E16 to E18) for 3 or 6 hours (39.5°C) had an immediate stimulatory effect on myoblast proliferation that lasted for up to two weeks post-hatch; this was followed by increased hypertrophy at later ages. The various incubation temperatures and TM durations focused on the fine-tuning of muscle development and growth processes during late-term embryogenesis as well as in post-hatch chickens.
APA, Harvard, Vancouver, ISO, and other styles
You might also be interested in the extended bibliographies on the topic 'Myoblasts' for particular source types:
Journal articles Dissertations / Theses Books
We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!

To the bibliography