High final energy of gallium arsenide laser increases MyoD gene expression during the intermediate phase of muscle regeneration after cryoinjury in rats

We show here that the distal regulatory region (DRR) of the mouse and human MyoD gene contains a conserved SRF binding CArG-like element. In electrophoretic mobility shift assays with myoblast nuclear extracts, this CArG sequence, although slightly divergent, bound two complexes containing, respectively, the transcription factor YY1 and SRF associated with the acetyltransferase CBP and members of C/EBP family. A single nucleotide mutation in the MyoD-CArG element suppressed binding of both SRF and YY1 complexes and abolished DRR enhancer activity in stably transfected myoblasts. This MyoD-CArG sequence is active in modulating endogeneous MyoD gene expression because microinjection of oligonucleotides corresponding to the MyoD-CArG sequence specifically and rapidly suppressed MyoD expression in myoblasts. In vivo, the expression of a transgenic construct comprising a minimal MyoD promoter fused to the DRR and β-galactosidase was induced with the same kinetics as MyoD during mouse muscle regeneration. In contrast induction of this reporter was no longer seen in regenerating muscle from transgenic mice carrying a mutated DRR-CArG. These results show that an SRF binding CArG element present in MyoD gene DRR is involved in the control of MyoD gene expression in skeletal myoblasts and in mature muscle satellite cell activation during muscle regeneration.

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bHLH transcription factor MyoD affects myosin heavy chain expression pattern in a muscle-specific fashion

AJP Cell Physiology ◽

10.1152/ajpcell.2001.280.2.c408 ◽

2001 ◽

Vol 280 (2) ◽

pp. C408-C413 ◽

Cited By ~ 38

Author(s):

David J. Seward ◽

John C. Haney ◽

Michael A. Rudnicki ◽

Steven J. Swoap

Keyword(s):

Gene Expression ◽

Myosin Heavy Chain ◽

Heavy Chain ◽

Biceps Brachii ◽

Bhlh Transcription Factor ◽

Hindlimb Unweighting ◽

Protein Pool ◽

In The Wild ◽

Myod Gene ◽

Mhc Iib

A strong correlative pattern between MyoD gene expression and myosin heavy chain IIB (MHC IIB) gene expression exists. To test whether this correlative relationship is causative, MHC gene expression in muscles from MyoD(−/−) mice was analyzed. The MHC IIB gene was not detectable in the MyoD(−/−) diaphragm, whereas the MHC IIB protein made up 10.0 ± 1.7% of the MHC protein pool in the wild-type (WT) mouse diaphragm. Furthermore, the MHC IIA protein was not detectable in the MyoD(−/−) biceps brachii, and the MHC IIB protein was overexpressed in the masseter. To examine whether MyoD is required for the upregulation of the MHC IIB gene within slow muscle after disuse, MyoD(−/−) and WT hindlimb musculature was unweighted. MyoD(−/−) exhibited a diminished response in the upregulation of the MHC IIB mRNA within the soleus muscle as a result of the hindlimb unweighting. Collectively, these data suggest that MyoD plays a role in the MHC profile in a muscle-specific fashion.

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Adenovirus Late-Phase Infection Is Controlled by a Novel L4 Promoter

Journal of Virology ◽

10.1128/jvi.00107-10 ◽

2010 ◽

Vol 84 (14) ◽

pp. 7096-7104 ◽

Cited By ~ 22

Author(s):

Susan J. Morris ◽

Gillian E. Scott ◽

Keith N. Leppard

Keyword(s):

Gene Expression ◽

Intermediate Phase ◽

Expression Patterns ◽

Late Phase ◽

Adenovirus Vector ◽

Human Adenovirus ◽

Late Gene ◽

Genome Replication ◽

Late Gene Expression ◽

Viral Genome Replication

ABSTRACT During human adenovirus 5 infection, a temporal cascade of gene expression leads ultimately to the production of large amounts of the proteins needed to construct progeny virions. However, the mechanism for the activation of the major late gene that encodes these viral structural proteins has not been well understood. We show here that two key positive regulators of the major late gene, L4-22K and L4-33K, previously thought to be expressed under the control of the major late promoter itself, initially are expressed from a novel promoter that is embedded within the major late gene and dedicated to their expression. This L4 promoter is required for late gene expression and is activated by a combination of viral protein activators produced during the infection, including E1A, E4 Orf3, and the intermediate-phase protein IVa2, and also by viral genome replication. This new understanding redraws the long-established view of how adenoviral gene expression patterns are controlled and offers new ways to manipulate that gene expression cascade for adenovirus vector applications.

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Anabolic Steroid Administration and Growth Related Gene Expression During Muscle Regeneration

Medicine & Science in Sports & Exercise ◽

10.1249/01.mss.0000323215.56532.da ◽

2008 ◽

Vol 40 (Supplement) ◽

pp. S314-S315

Author(s):

James P. White ◽

Raymond W. Thompson ◽

Kristen A. Baltgalvis ◽

James A. Carson

Keyword(s):

Gene Expression ◽

Anabolic Steroid ◽

Muscle Regeneration ◽

Related Gene ◽

Steroid Administration

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The Regulation of MyoD Gene Expression: Conserved Elements Mediate Expression in Embryonic Axial Muscle

Developmental Biology ◽

10.1006/dbio.1995.1290 ◽

1995 ◽

Vol 171 (2) ◽

pp. 386-398 ◽

Cited By ~ 75

Author(s):

Atsushi Asakura ◽

Gary E. Lyons ◽

Stephen J. Tapscott

Keyword(s):

Gene Expression ◽

Axial Muscle ◽

Myod Gene

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Estrogen receptor regulates MyoD gene expression by preventing AP-1-mediated repression

Biochemical and Biophysical Research Communications ◽

10.1016/j.bbrc.2009.08.153 ◽

2009 ◽

Vol 389 (2) ◽

pp. 360-365 ◽

Cited By ~ 11

Author(s):

G. Pedraza-Alva ◽

J.M. Zingg ◽

A. Donda ◽

L. Pérez-Martínez

Keyword(s):

Gene Expression ◽

Estrogen Receptor ◽

Myod Gene

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Foxk1 recruits the Sds3 complex and represses gene expression in myogenic progenitors

Biochemical Journal ◽

10.1042/bj20120563 ◽

2012 ◽

Vol 446 (3) ◽

pp. 349-357 ◽

Cited By ~ 22

Author(s):

Xiaozhong Shi ◽

David C. Seldin ◽

Daniel J. Garry

Keyword(s):

Gene Expression ◽

Cell Cycle ◽

Skeletal Muscle ◽

Protein Kinase ◽

Muscle Regeneration ◽

Cell Cycle Progression ◽

Adaptor Protein ◽

Skeletal Muscle Regeneration ◽

Cycle Progression ◽

Repression Complex

Previous studies have established that Foxk1 (forkhead box k1) plays an important role in skeletal muscle regeneration. Foxk1 regulates the cell-cycle progression of myogenic progenitors by repressing the cell-cycle inhibitor gene p21. However, the underlying mechanism is not well understood. In the present study, we report the identification of Sds3 (suppressor of defective silencing 3) as an adaptor protein that recruits the Sin3 [SWI (switch)-independent 3]–HDAC (histone deacetylase) repression complex and binds Foxk1. Using GST (glutathione transferase) pull-down assays, we defined the interaction between the Foxk1 FHA (forkhead-associated domain) domain and phospho-Thr49 in Sds3. We demonstrated that the transcriptional repression of Foxk1 is dependent on the Sin3–Sds3 repression complex, and knockdown of Sds3 results in cell-cycle arrest. We further identified the protein kinase CK2 as the protein kinase for Sds3 Thr49 and demonstrated that the protein kinase activity of CK2 is required for proper cell-cycle progression. Analysis of CK2 mutant mice reveals perturbation of skeletal muscle regeneration due to the dysregulation of cell-cycle kinetics. Overall, these studies define a CK2–Sds3–Foxk1 cascade that modulates gene expression and regulates skeletal muscle regeneration.

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Studies of the dynamics of skeletal muscle regeneration: the mouse came back!

Biochemistry and Cell Biology ◽

10.1139/o98-007 ◽

1998 ◽

Vol 76 (1) ◽

pp. 13-26 ◽

Cited By ~ 35

Author(s):

Judy E Anderson

Keyword(s):

Gene Expression ◽

Skeletal Muscle ◽

Magnetic Resonance ◽

Magnetic Resonance Spectroscopy ◽

Muscle Fiber ◽

Muscle Regeneration ◽

Skeletal Muscle Regeneration ◽

Resonance Spectroscopy ◽

Dystrophic Mouse

Regeneration of skeletal muscle tissue includes sequential processes of muscle cell proliferation and commitment, cell fusion, muscle fiber differentiation, and communication between cells of various tissues of origin. Central to the process is the myosatellite cell, a quiescent precursor cell located between the mature muscle fiber and its sheath of external lamina. To form new fibers in a muscle damaged by disease or direct injury, satellite cells must be activated, proliferate, and subsequently fuse into an elongated multinucleated cell. Current investigations in the field concern modulation of the effectiveness of skeletal muscle regeneration, the regeneration-specific role of myogenic regulatory gene expression distinct from expression during development, the impact of growth and scatter factors and their respective receptors in amplifying precursor numbers, and promoting fusion and maturation of new fibers and the ultimate clinical therapeutic applications of such information to alleviate disease. One approach to muscle regeneration integrates observations of muscle gene expression, proliferation, myoblast fusion, and fiber growth in vivo with parallel studies of cell cycling behaviour, endocrine perturbation, and potential biochemical markers of steps in the disease-repair process detected by magnetic resonance spectroscopy techniques. Experiments on muscles from limb, diaphragm, and heart of the mdx dystrophic mouse, made to parallel clinical trials on human Duchenne muscular dystrophy, help to elucidate mechanisms underlying the positive treatment effects of the glucocorticoid drug deflazacort. This review illustrates an effective combination of in vivo and in vitro experiments to integrate the distinctive complexities of post-natal myogenesis in regeneration of skeletal muscle tissue.Key words: satellite cell, cell cycling, HGF/SF, c-met receptor, MyoD, myogenin, magnetic resonance spectroscopy, mdx dystrophic mouse, deflazacort.

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EM.P.3.06 Transient upregulation of matrilin-2 gene expression suggests a role in early steps of skeletal muscle regeneration

Neuromuscular Disorders ◽

10.1016/j.nmd.2009.06.103 ◽

2009 ◽

Vol 19 (8-9) ◽

pp. 575-576

Author(s):

É. Korpos ◽

L. Mátés ◽

L. Mendler ◽

M. Kiricsi ◽

Á. Zvara ◽

...

Keyword(s):

Gene Expression ◽

Skeletal Muscle ◽

Muscle Regeneration ◽

Skeletal Muscle Regeneration

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OR-009 The expression and roles of lncRNAs in the regeneration of skeletal muscle contusion

Exercise Biochemistry Review ◽

10.14428/ebr.v1i2.8693 ◽

2018 ◽

Vol 1 (2) ◽

Author(s):

Lifang Zheng ◽

Peijie Chen ◽

Weihua Xiao

Keyword(s):

Gene Expression ◽

Skeletal Muscle ◽

Muscle Regeneration ◽

Myoblast Differentiation ◽

Control Group ◽

Myogenic Regulatory Factors ◽

Post Injury ◽

Regulatory Factors ◽

Expression Levels ◽

Skeletal Muscle Contusion

Objective In recent years, Accumulating evidence from myoblast differentiation in vitro, cardiotoxin (CTX)-mediated injury or mdx mice suggested that some lncRNAs such as Malat1, H19, linc-MD1, linc-YY1, Sirt1 AS and lnc-mg may modulate myogenesis and muscle regeneration. However, the change of lncRNAs in skeletal muscle contusion and their possible roles are still unclear. We hypothesize that the lncRNAs may be involved in the repair of skeletal muscle contusion. Methods Forty C57BL/6 male mice were randomly divided into two groups, uninjured control group (group C) and muscle contusion group (group S). The mice of group S suffered from contusion injury. All the mice were killed to harvest gastrocnemius at 3, 6, 12 and 24 days post-injury. The gene expression were detected by PCR technique. Gastrocnemius were stained with H & E to evaluate the general morphology. Data were analyzed by One-way analysis of variance, with statistical significance being set at p ≤ 0.05. Results The expression levels of linc-MD1 and Sirt1 AS were significantly higher than that of the uninjured control group at 3, 6 and 12 days post-injury (p<0.01). And Malat1 was highly expressed in the skeletal muscle of the muscle contusion group at 3 days post-injury and continuously up-regulated at 6 days (p<0.01). Moreover, linc-YY1 and H19 were all elevated significantly at 6 days (all p<0.01), but their gene expression levels did not change significantly at 3, 12 and 24 days post-injury, as compared to the uninjured control group. Furthermore, lnc-mg mRNA level did not change significantly in the whole process of regeneration after muscle contusion except the time point of 12 days post-injury which decreased significantly (p<0.01). The expression of myogenic regulatory factors (MyoD, myogenin, myf5, myf6) were studied, they were all elevated significantly at 3 and 6 days (all p<0.01; except myogenin ), and returned to normal at 24 days post-injury, as compared to the uninjured control group. Meanwhile, Pearson correlations showed that there was an correlation between lincRNAs and myogenic regulatory factors mentioned above. Conclusions The expression of myogenic regulatory factors increased significantly after muscle contusion. Meanwhile, varieties of lncRNAs (Malat1, H19, lnc-mg, linc-MD1, linc-YY1, Sirt1 AS) were also up-regulated. Moreover, there was correlation between lncRNAs and myogenic regulatory factors for skeletal muscle regeneration. These results suggest that lncRNAs may play important roles in the regeneration of skeletal muscle contusion.

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