scholarly journals Age-Related Decreases of Serum-Response Factor Levels in Human Mesenchymal Stem Cells Are Involved in Skeletal Muscle Differentiation and Engraftment Capacity

2014 ◽  
Vol 23 (11) ◽  
pp. 1206-1216 ◽  
Author(s):  
Chiao-Hsuan Ting ◽  
Pai-Jiun Ho ◽  
Betty Linju Yen
Keyword(s):  
Skeletal Muscle ◽  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Serum Response Factor ◽  
Human Mesenchymal Stem Cells ◽  
Muscle Differentiation ◽  
Response Factor ◽  
Skeletal Muscle Differentiation ◽  
Age Related ◽  
Serum Response

scholarly journals Enhancer of Polycomb1 Acts on Serum Response Factor to Regulate Skeletal Muscle Differentiation

2009 ◽  
Vol 284 (24) ◽  
pp. 16308-16316 ◽  
Author(s):  
Ju-Ryoung Kim ◽  
Hae Jin Kee ◽  
Ji-Young Kim ◽  
Hosouk Joung ◽  
Kwang-Il Nam ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Serum Response Factor ◽  
Muscle Differentiation ◽  
Specific Gene ◽  
Response Factor ◽  
Gene Promoters ◽  
Skeletal Muscle Differentiation ◽  
Actin Promoter ◽  
Myoblast Cells ◽  
Serum Response

Skeletal muscle differentiation is well regulated by a series of transcription factors. We reported previously that enhancer of polycomb1 (Epc1), a chromatin protein, can modulate skeletal muscle differentiation, although the mechanisms of this action have yet to be defined. Here we report that Epc1 recruits both serum response factor (SRF) and p300 to induce skeletal muscle differentiation. Epc1 interacted physically with SRF. Transfection of Epc1 to myoblast cells potentiated the SRF-induced expression of skeletal muscle-specific genes as well as multinucleation. Proximal CArG box in the skeletal α-actin promoter was responsible for the synergistic activation of the promoter-luciferase. Epc1 knockdown caused a decrease in the acetylation of histones associated with serum response element (SRE) of the skeletal α-actin promoter. The Epc1·SRF complex bound to the SRE, and the knockdown of Epc1 resulted in a decrease in SRF binding to the skeletal α-actin promoter. Epc1 recruited histone acetyltransferase activity, which was potentiated by cotransfection with p300 but abolished by si-p300. Epc1 directly bound to p300 in myoblast cells. Epc1+/− mice showed distortion of skeletal α-actin, and the isolated myoblasts from the mice had impaired muscle differentiation. These results suggest that Epc1 is required for skeletal muscle differentiation by recruiting both SRF and p300 to the SRE of muscle-specific gene promoters.

scholarly journals SRF is a nonhistone methylation target of KDM2B and SET7 in the regulation of skeletal muscle differentiation

2021 ◽  
Vol 53 (2) ◽  
pp. 250-263
Author(s):  
Duk-Hwa Kwon ◽  
Joo-Young Kang ◽  
Hosouk Joung ◽  
Ji-Young Kim ◽  
Anna Jeong ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Cell Differentiation ◽  
Muscle Cell ◽  
Transcriptional Activation ◽  
Serum Response Factor ◽  
Muscle Differentiation ◽  
Skeletal Muscle Differentiation ◽  
Muscle Cell Differentiation ◽  
Lysine Residues ◽  
Serum Response

AbstractThe demethylation of histone lysine residues, one of the most important modifications in transcriptional regulation, is associated with various physiological states. KDM2B is a demethylase of histones H3K4, H3K36, and H3K79 and is associated with the repression of transcription. Here, we present a novel mechanism by which KDM2B demethylates serum response factor (SRF) K165 to negatively regulate muscle differentiation, which is counteracted by the histone methyltransferase SET7. We show that KDM2B inhibited skeletal muscle differentiation by inhibiting the transcription of SRF-dependent genes. Both KDM2B and SET7 regulated the balance of SRF K165 methylation. SRF K165 methylation was required for the transcriptional activation of SRF and for the promoter occupancy of SRF-dependent genes. SET7 inhibitors blocked muscle cell differentiation. Taken together, these data indicate that SRF is a nonhistone target of KDM2B and that the methylation balance of SRF as maintained by KDM2B and SET7 plays an important role in muscle cell differentiation.

scholarly journals Serum Response Factor in muscle tissues: from development to ageing

2016 ◽  
Vol 26 (2) ◽  
Author(s):  
Dario Coletti ◽  
Nissrine Daou ◽  
Medhi Hassani ◽  
Zhenlin Li ◽  
Ara Parlakian
Keyword(s):  
Skeletal Muscle ◽  
Serum Response Factor ◽  
Molecular Level ◽  
Response Factor ◽  
Actin Isoforms ◽  
Common Features ◽  
Age Related ◽  
Muscle Tissues ◽  
Characteristic Features ◽  
Serum Response

Skeletal, cardiac and smooth muscle cells share various common characteristic features. During development the embryonic mesodermal layer contribute at different proportions to the formation of these tissues. At the functional level, contractility as well as its decline during ageing, are also common features. Cytoskeletal components of these tissues are characterized by various actin isoforms that govern through their status (polymerised versus monomeric) and their interaction with the myosins the contractile properties of these muscles. Finally, at the molecular level, a set of different transcription factors with the notable exception of Serum Response Factor SRF- which is commonly enriched in the 3 types of muscle- drive and maintain the differentiation of these cells (Myf5, MyoD, Myogenin for skeletal muscle; Nkx2.5, GATA4 for cardiomyocytes). In this review, we will focus on the transcription factor SRF and its role in the homeostasis of cardiac, smooth and skeletal muscle tissues as well as its behaviour during the age related remodelling process of these tissues with a specific emphasis on animal models and human data when available.

scholarly journals Serum response factor p67SRF is expressed and required during myogenic differentiation of both mouse C2 and rat L6 muscle cell lines.

1992 ◽  
Vol 118 (6) ◽  
pp. 1489-1500 ◽  
Author(s):  
M Vandromme ◽  
C Gauthier-Rouvière ◽  
G Carnac ◽  
N Lamb ◽  
A Fernandez
Keyword(s):  
Skeletal Muscle ◽  
Cell Lines ◽  
Muscle Cell ◽  
Serum Response Factor ◽  
Troponin T ◽  
Myogenic Differentiation ◽  
Muscle Differentiation ◽  
Response Factor ◽  
Serum Response

The 67-kD serum response factor (p67SRF) is a ubiquitous nuclear transcription factor that acts by direct binding to a consensus DNA sequence, the serum response element (SRE), present in the promoter region of numerous genes. Although p67SRF was initially implicated in the activation of mitogen-stimulated genes, the identification of a sequence similar to SRE, the CArG box motif, competent to interact with SRE binding factors in many muscle-specific genes, has led to speculation that, in addition to its function in cell proliferation, p67SRF may play a role in muscle differentiation. Indirect immunofluorescence using affinity-purified antibodies specifically directed against p67SRF reveals that this factor is constitutively expressed and localized in the nucleus of two skeletal muscle cell lines: rat L6 and mouse C2 myogenic cells during myogenic differentiation. This result was further confirmed through immunoblotting and Northern blot analysis. Furthermore, specific inhibition of p67SRF in vivo through microinjection of purified p67SRF antibodies prevented the myoblast-myotube transition and the expression of muscle-specific genes such as the protein troponin T. We further showed that anti-p67SRF injection also inhibited the expression of the myogenic factor myogenin, implying an early requirement for p67SRF in muscle differentiation. These results demonstrate that p67SRF is involved in the process of skeletal muscle differentiation. The potential action of p67SRF via CArG sequences is discussed.

Galectin-1 Induces Skeletal Muscle Differentiation in Human Fetal Mesenchymal Stem Cells and Increases Muscle Regeneration

Stem Cells ◽  
2006 ◽  
Vol 24 (8) ◽  
pp. 1879-1891 ◽  
Author(s):  
Jerry Chan ◽  
Keelin O'Donoghue ◽  
Manuela Gavina ◽  
Yvan Torrente ◽  
Nigel Kennea ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Muscle Regeneration ◽  
Muscle Differentiation ◽  
Skeletal Muscle Differentiation

scholarly journals Chronic senescent human mesenchymal stem cells as possible contributor to the wound healing disorder after exposure to the alkylating agent sulfur mustard

2021 ◽  
Vol 95 (2) ◽  
pp. 727-747
Author(s):  
Simone Rothmiller ◽  
Niklas Jäger ◽  
Nicole Meier ◽  
Thimo Meyer ◽  
Adrian Neu ◽  
...  
Keyword(s):  
Stem Cells ◽  
Wound Healing ◽  
Mesenchymal Stem Cells ◽  
Alkylating Agent ◽  
Chronic Wounds ◽  
Sulfur Mustard ◽  
Morphological Changes ◽  
Human Mesenchymal Stem Cells ◽  
Age Related

AbstractWound healing is a complex process, and disturbance of even a single mechanism can result in chronic ulcers developing after exposure to the alkylating agent sulfur mustard (SM). A possible contributor may be SM-induced chronic senescent mesenchymal stem cells (MSCs), unable to fulfil their regenerative role, by persisting over long time periods and creating a proinflammatory microenvironment. Here we show that senescence induction in human bone marrow derived MSCs was time- and concentration-dependent, and chronic senescence could be verified 3 weeks after exposure to between 10 and 40 µM SM. Morphological changes, reduced clonogenic and migration potential, longer scratch closure times, differences in senescence, motility and DNA damage response associated genes as well as increased levels of proinflammatory cytokines were revealed. Selective removal of these cells by senolytic drugs, in which ABT-263 showed initial potential in vitro, opens the possibility for an innovative treatment strategy for chronic wounds, but also tumors and age-related diseases.

scholarly journals Skeletal Muscle-Derived Human Mesenchymal Stem Cells: Influence of Different Culture Conditions on Proliferative and Myogenic Capabilities

2020 ◽  
Vol 11 ◽  
Author(s):  
Stefano Testa ◽  
Carles Sánchez Riera ◽  
Ersilia Fornetti ◽  
Federica Riccio ◽  
Claudia Fuoco ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Human Mesenchymal Stem Cells ◽  
Culture Conditions

scholarly journals Insulin-Like Growth Factor Binding Protein-6 Promotes the Differentiation of Placental Mesenchymal Stem Cells into Skeletal Muscle Independent of Insulin-Like Growth Factor Receptor-1 and Insulin Receptor

2019 ◽  
Vol 2019 ◽  
pp. 1-18 ◽  
Author(s):  
Doaa Aboalola ◽  
Victor K. M. Han
Keyword(s):  
Skeletal Muscle ◽  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Growth Factor ◽  
Muscle Differentiation ◽  
Insulin Like Growth Factor ◽  
Differentiation Process ◽  
Placental Mesenchymal Stem Cells

As mesenchymal stem cells (MSCs) are being investigated for regenerative therapies to be used in the clinic, delineating the roles of the IGF system in MSC growth and differentiation, in vitro, is vital in developing these cellular therapies to treat degenerative diseases. Muscle differentiation is a multistep process, starting with commitment to the muscle lineage and ending with the formation of multinucleated fibers. Insulin-like growth factor binding protein-6 (IGFBP-6), relative to other IGFBPs, has high affinity for IGF-2. However, the role of IGFBP-6 in muscle development has not been clearly defined. Our previous studies showed that in vitro extracellular IGFBP-6 increased myogenesis in early stages and could enhance the muscle differentiation process in the absence of IGF-2. In this study, we identified the signal transduction mechanisms of IGFBP-6 on muscle differentiation by placental mesenchymal stem cells (PMSCs). We showed that muscle differentiation required activation of both AKT and MAPK pathways. Interestingly, we demonstrated that IGFBP-6 could compensate for IGF-2 loss and help enhance the muscle differentiation process by triggering predominantly the MAPK pathway independent of activating either IGF-1R or the insulin receptor (IR). These findings indicate the complex interactions between IGFBP-6 and IGFs in PMSC differentiation into the skeletal muscle and that the IGF signaling axis, specifically involving IGFBP-6, is important in muscle differentiation. Moreover, although the major role of IGFBP-6 is IGF-2 inhibition, it is not necessarily the case that IGFBP-6 is the main modulator of IGF-2.

scholarly journals The Cytoskeleton-associated PDZ-LIM Protein, ALP, Acts on Serum Response Factor Activity to Regulate Muscle Differentiation

2007 ◽  
Vol 18 (5) ◽  
pp. 1723-1733 ◽  
Author(s):  
Pascal Pomiès ◽  
Mohammad Pashmforoush ◽  
Cristina Vegezzi ◽  
Kenneth R. Chien ◽  
Charles Auffray ◽  
...  
Keyword(s):  
Serum Response Factor ◽  
Critical Role ◽  
Muscle Differentiation ◽  
Actin Dynamics ◽  
Response Factor ◽  
Cytoskeletal Regulation ◽  
Expression Construct ◽  
Filament Bundles ◽  
Serum Response

In this report, an antisense RNA strategy has allowed us to show that disruption of ALP expression affects the expression of the muscle transcription factors myogenin and MyoD, resulting in the inhibition of muscle differentiation. Introduction of a MyoD expression construct into ALP-antisense cells is sufficient to restore the capacity of the cells to differentiate, illustrating that ALP function occurs upstream of MyoD. It is known that MyoD is under the control of serum response factor (SRF), a transcriptional regulator whose activity is modulated by actin dynamics. A dramatic reduction of actin filament bundles is observed in ALP-antisense cells and treatment of these cells with the actin-stabilizing drug jasplakinolide stimulates SRF activity and restores the capacity of the cells to differentiate. Furthermore, we show that modulation of ALP expression influences SRF activity, the level of its coactivator, MAL, and muscle differentiation. Collectively, these results suggest a critical role of ALP on muscle differentiation, likely via cytoskeletal regulation of SRF.

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