scholarly journals STIM1 as a key regulator for Ca2+ homeostasis in skeletal-muscle development and function

2011 ◽  
Vol 1 (1) ◽  
pp. 16 ◽  
Author(s):  
Santeri Kiviluoto ◽  
Jean-Paul Decuypere ◽  
Humbert De Smedt ◽  
Ludwig Missiaen ◽  
Jan B Parys ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Muscle Development ◽  
Skeletal Muscle Development ◽  
And Function

Growing healthy muscles to optimise metabolic health into adult life

2014 ◽  
Vol 5 (6) ◽  
pp. 420-434 ◽  
Author(s):  
S. A. Bayol ◽  
C. R. Bruce ◽  
G. D. Wadley
Keyword(s):  
Skeletal Muscle ◽  
Muscle Development ◽  
Maternal Obesity ◽  
Adult Life ◽  
Metabolic Health ◽  
Skeletal Muscle Development ◽  
Pregnancy And Lactation ◽  
Functional Consequences ◽  
And Function

The importance of skeletal muscle for metabolic health and obesity prevention is gradually gaining recognition. As a result, interventions are being developed to increase or maintain muscle mass and metabolic function in adult and elderly populations. These interventions include exercise, hormonal and nutritional therapies. Nonetheless, growing evidence suggests that maternal malnutrition and obesity during pregnancy and lactation impede skeletal muscle development and growth in the offspring, with long-term functional consequences lasting into adult life. Here we review the role of skeletal muscle in health and obesity, providing an insight into how this tissue develops and discuss evidence that maternal obesity affects its development, growth and function into adult life. Such evidence warrants the need to develop early life interventions to optimise skeletal muscle development and growth in the offspring and thereby maximise metabolic health into adult life.

scholarly journals Cavin4b/Murcb Is Required for Skeletal Muscle Development and Function in Zebrafish

PLoS Genetics ◽  
2016 ◽  
Vol 12 (6) ◽  
pp. e1006099 ◽  
Author(s):  
Michael P. Housley ◽  
Brian Njaine ◽  
Filomena Ricciardi ◽  
Oliver A. Stone ◽  
Soraya Hölper ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Muscle Development ◽  
Skeletal Muscle Development ◽  
And Function

Impaired skeletal muscle development and function in male, but not female, genomic androgen receptor knockout mice

2008 ◽  
Vol 22 (8) ◽  
pp. 2676-2689 ◽  
Author(s):  
Helen E. MacLean ◽  
W. S. Maria Chiu ◽  
Amanda J. Notini ◽  
Anna-Maree Axell ◽  
Rachel A. Davey ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Androgen Receptor ◽  
Knockout Mice ◽  
Muscle Development ◽  
Skeletal Muscle Development ◽  
And Function

scholarly journals Differential physiological role of BIN1 isoforms in skeletal muscle development, function and regeneration

2018 ◽  
Author(s):  
Ivana Prokic ◽  
Belinda Cowling ◽  
Candice Kutchukian ◽  
Christine Kretz ◽  
Hichem Tasfaout ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Muscle Regeneration ◽  
Muscle Development ◽  
Physiological Role ◽  
Membrane Remodeling ◽  
Skeletal Muscle Development ◽  
Developmental Defects ◽  
Intracellular Organization ◽  
And Function

AbstractSkeletal muscle development and regeneration are tightly regulated processes. How the intracellular organization of muscle fibers is achieved during these steps is unclear. Here we focus on the cellular and physiological roles of amphiphysin 2 (BIN1), a membrane remodeling protein mutated in both congenital and adult centronuclear myopathies, that is ubiquitously expressed and has skeletal muscle-specific isoforms. We created and characterized constitutive, muscle-specific and inducible Bin1 homozygous and heterozygous knockout mice targeting either ubiquitous or muscle-specific isoforms. Constitutive Bin1-deficient mice died at birth from lack of feeding due to a skeletal muscle defect. T-tubules and other organelles were misplaced and altered, supporting a general early role of BIN1 on intracellular organization in addition to membrane remodeling. Whereas restricted deletion of Bin1 in unchallenged adult muscles had no impact, the forced switch from the muscle-specific isoforms to the ubiquitous isoforms through deletion of the in-frame muscle–specific exon delayed muscle regeneration. Thus, BIN1 ubiquitous function is necessary for muscle development and function while its muscle-specific isoforms fine-tune muscle regeneration in adulthood, supporting that BIN1 centronuclear myopathy with congenital onset are due to developmental defects while later onset may be due to regeneration defects.

scholarly journals Differential physiological roles for BIN1 isoforms in skeletal muscle development, function and regeneration

2020 ◽  
Vol 13 (11) ◽  
pp. dmm044354
Author(s):  
Ivana Prokic ◽  
Belinda S. Cowling ◽  
Candice Kutchukian ◽  
Christine Kretz ◽  
Hichem Tasfaout ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Muscle Regeneration ◽  
Muscle Development ◽  
Membrane Remodeling ◽  
Skeletal Muscle Development ◽  
Developmental Defects ◽  
Intracellular Organization ◽  
T Tubules ◽  
And Function ◽  
Fine Tune

ABSTRACTSkeletal muscle development and regeneration are tightly regulated processes. How the intracellular organization of muscle fibers is achieved during these steps is unclear. Here, we focus on the cellular and physiological roles of amphiphysin 2 (BIN1), a membrane remodeling protein mutated in both congenital and adult centronuclear myopathies (CNM), that is ubiquitously expressed and has skeletal muscle-specific isoforms. We created and characterized constitutive muscle-specific and inducible Bin1 homozygous and heterozygous knockout mice targeting either ubiquitous or muscle-specific isoforms. Constitutive Bin1-deficient mice died at birth from lack of feeding due to a skeletal muscle defect. T-tubules and other organelles were misplaced and altered, supporting a general early role for BIN1 in intracellular organization, in addition to membrane remodeling. Although restricted deletion of Bin1 in unchallenged adult muscles had no impact, the forced switch from the muscle-specific isoforms to the ubiquitous isoforms through deletion of the in-frame muscle-specific exon delayed muscle regeneration. Thus, ubiquitous BIN1 function is necessary for muscle development and function, whereas its muscle-specific isoforms fine tune muscle regeneration in adulthood, supporting that BIN1 CNM with congenital onset are due to developmental defects, whereas later onset may be due to regeneration defects.

scholarly journals Longitudinal epi-transcriptome profiling reveals the crucial role of m6A in prenatal skeletal muscle development of pigs

2019 ◽  
Author(s):  
Xinxin Zhang ◽  
Yilong Yao ◽  
Jinghua Han ◽  
Yalan Yang ◽  
Yun Chen ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Muscle Development ◽  
Transcriptome Profiling ◽  
Rna Modification ◽  
C2c12 Myoblast ◽  
Skeletal Muscle Development ◽  
The Status ◽  
The Stability ◽  
Myoblast Cells ◽  
And Function

AbstractBackgroundN6-methyladenosine (m6A) is the most abundant RNA modification and essentially participates in the regulation of skeletal muscle development. However, the status and function of m6A methylation in prenatal myogenesis remains unclear now.ResultsIn our present study, we first demonstrate that chemical suppression of m6A and knockdown METTL14 significantly inhibit the differentiation and promote the proliferation of C2C12 myoblast cells. The mRNA expression of m6A reader protein IGF2BP1, which functions to promote the stability of target mRNA, continually decreases during the prenatal skeletal muscle development. Thereafter, profiling transcriptome-wide m6A for six developmental stage of prenatal skeletal muscle, which spanning two important waves of pig myogenesis, were performed using a refined MeRIP sequencing technology that is optimal for small-amount of RNA samples. Highly dynamic m6A methylomes across different development stages were then revealed, with majority of the affected genes enriched in pathways of skeletal muscle development. In association with the transcriptome-wide alterations, transcriptional regulatory factors (MyoD) and differentiated markers (MyHC, MYH1) of muscle development are simultaneously regulated with m6A and IGF2BP1. Knockdown of IGF2BP1 also suppresses myotube formation and promotes cell proliferation.ConclusionsThe present study clarifies the dynamics of RNA m6A methylation in the regulation of prenatal skeletal muscle development, providing a data baseline for future developmental as well as biomedical studies of m6A functions in muscle development and disease.

scholarly journals Tiny Regulators of Massive Tissue: MicroRNAs in Skeletal Muscle Development, Myopathies, and Cancer Cachexia

2020 ◽  
Vol 10 ◽  
Author(s):  
Gurinder Bir Singh ◽  
Douglas B Cowan ◽  
Da-Zhi Wang
Keyword(s):  
Gene Expression ◽  
Skeletal Muscle ◽  
Cancer Cachexia ◽  
Muscle Development ◽  
Loss Of Function ◽  
Skeletal Muscle Development ◽  
Muscle Disorders ◽  
Muscle Biology ◽  
And Function

Skeletal muscles are the largest tissues in our body and the physiological function of muscle is essential to every aspect of life. The regulation of development, homeostasis, and metabolism is critical for the proper functioning of skeletal muscle. Consequently, understanding the processes involved in the regulation of myogenesis is of great interest. Non-coding RNAs especially microRNAs (miRNAs) are important regulators of gene expression and function. MiRNAs are small (~22 nucleotides long) noncoding RNAs known to negatively regulate target gene expression post-transcriptionally and are abundantly expressed in skeletal muscle. Gain- and loss-of function studies have revealed important roles of this class of small molecules in muscle biology and disease. In this review, we summarize the latest research that explores the role of miRNAs in skeletal muscle development, gene expression, and function as well as in muscle disorders like sarcopenia and Duchenne muscular dystrophy (DMD). Continuing with the theme of the current review series, we also briefly discuss the role of miRNAs in cancer cachexia.

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