STAT3 Regulates Self-Renewal of Adult Muscle Satellite Cells during Injury-Induced Muscle Regeneration

Zhu, Han; Xiao, Fang; Wang, Gang; Wei, Xiuqing; Jiang, Lei; Chen, Yan; Zhu, Lin; Wang, Haixia; Diao, Yarui; Wang, Hua-Ting; Ip, Nancy Y.; Cheung, Tom H.; Wu, Zhenguo

doi:10.1016/j.celrep.2016.07.041

Cited by 50 publications

(40 citation statements)

References 67 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The chemical inhibitors and siRNA used in the studies above could have off-target effects, thus limiting the interpretation that their results were only due to the effects of STAT3 in muscle satellite cells [21]. Moreover, since STAT3 is ubiquitously expressed, STAT3 inhibitors could have influenced muscle regeneration due to the effects of STAT3 inhibition in different cell types and not only due to its effect on satellite cells [21].…”

Section: Stat3 Modulates Satellite Cell Myogenic Capacity and Selfmentioning

confidence: 99%

“…Moreover, since STAT3 is ubiquitously expressed, STAT3 inhibitors could have influenced muscle regeneration due to the effects of STAT3 inhibition in different cell types and not only due to its effect on satellite cells [21]. To better address the role of STAT3 in adult muscle satellite cells, a mouse model with a conditional deletion of STAT3 only in muscle satellite cells was generated.…”

Section: Stat3 Modulates Satellite Cell Myogenic Capacity and Selfmentioning

confidence: 99%

“…To better address the role of STAT3 in adult muscle satellite cells, a mouse model with a conditional deletion of STAT3 only in muscle satellite cells was generated. Conditional knockdown of STAT3 in muscle satellite cells did not affect normal muscle development or the number of Pax7+ satellite cells in muscles from STAT3 knockout (KO) mice compared to WT mice [21]. To evaluate the effects of muscle satellite cell STAT3 KO in muscle regeneration, different muscles were injured with cardiotoxin [21].…”

Section: Stat3 Modulates Satellite Cell Myogenic Capacity and Selfmentioning

confidence: 99%

“…Conditional knockdown of STAT3 in muscle satellite cells did not affect normal muscle development or the number of Pax7+ satellite cells in muscles from STAT3 knockout (KO) mice compared to WT mice [21]. To evaluate the effects of muscle satellite cell STAT3 KO in muscle regeneration, different muscles were injured with cardiotoxin [21]. Cardiotoxin injected muscles from STAT3 KO mice only demonstrated a defect in muscle regeneration 5 days post-injury, as shown by increased degeneration and fewer regenerated fibers at the site of injury [21].…”

Section: Stat3 Modulates Satellite Cell Myogenic Capacity and Selfmentioning

confidence: 99%

“…To evaluate the effects of muscle satellite cell STAT3 KO in muscle regeneration, different muscles were injured with cardiotoxin [21]. Cardiotoxin injected muscles from STAT3 KO mice only demonstrated a defect in muscle regeneration 5 days post-injury, as shown by increased degeneration and fewer regenerated fibers at the site of injury [21]. Moreover, cardiotoxin injured muscles from STAT3 KO mice had 50% fewer Pax7+ satellite cells compared to muscles from WT mice, which suggested that STAT3 plays a critical role in satellite cell self-renewal [21].…”

Section: Stat3 Modulates Satellite Cell Myogenic Capacity and Selfmentioning

confidence: 99%

See 4 more Smart Citations

STAT3 in Skeletal Muscle Function and Disorders

Guadagnin

Mázala

Chen

2018

IJMS

View full text Add to dashboard Cite

Signal transducer and activator of transcription 3 (STAT3) signaling plays critical roles in regulating skeletal muscle mass, repair, and diseases. In this review, we discuss the upstream activators of STAT3 in skeletal muscles, with a focus on interleukin 6 (IL6) and transforming growth factor beta 1 (TGF-β1). We will also discuss the double-edged effect of STAT3 activation in the muscles, including the role of STAT3 signaling in muscle hypertrophy induced by exercise training or muscle wasting in cachectic diseases and muscular dystrophies. STAT3 is a critical regulator of satellite cell self-renewal after muscle injury. STAT3 knock out affects satellite cell myogenic progression by impairing proliferation and inducing premature differentiation. Recent studies in STAT3 signaling demonstrated its direct role in controlling myogenic capacity of myoblasts and satellite cells, as well as the potential benefit in using STAT3 inhibitors to treat muscle diseases. However, prolonged STAT3 activation in muscles has been shown to be responsible for muscle wasting by activating protein degradation pathways. It is important to balance the extent of STAT3 activation and the duration and location (cell types) of the STAT3 signaling when developing therapeutic interventions. STAT3 signaling in other tissues and organs that can directly or indirectly affects skeletal muscle health are also discussed.

show abstract

Section: Stat3 Modulates Satellite Cell Myogenic Capacity and Selfmentioning

confidence: 99%

Section: Stat3 Modulates Satellite Cell Myogenic Capacity and Selfmentioning

confidence: 99%

Section: Stat3 Modulates Satellite Cell Myogenic Capacity and Selfmentioning

confidence: 99%

Section: Stat3 Modulates Satellite Cell Myogenic Capacity and Selfmentioning

confidence: 99%

Section: Stat3 Modulates Satellite Cell Myogenic Capacity and Selfmentioning

confidence: 99%

See 3 more Smart Citations

STAT3 in Skeletal Muscle Function and Disorders

Guadagnin

Mázala

Chen

2018

IJMS

View full text Add to dashboard Cite

show abstract

Regulation of skeletal muscle stem cells by fibroblast growth factors

Pawlikowski

Vogler

Gadek

et al. 2017

Developmental Dynamics

138

123

View full text Add to dashboard Cite

Fibroblast growth factors (FGFs) are essential for self-renewal of skeletal muscle stem cells (satellite cells) and required for maintenance and repair of skeletal muscle. Satellite cells express high levels of FGF receptors 1 and 4, low levels of FGF receptor 3, and little or no detectable FGF receptor 2. Of the multiple FGFs that influence satellite cell function in culture, FGF2 and FGF6 are the only members that regulate satellite cell function in vivo by activating ERK MAPK, p38a/b MAPKs, PI3 kinase, PLCg and STATs. Regulation of FGF signaling is complex in satellite cells, requiring Syndecan-4, a heparan sulfate proteoglycan, as well as ß1-integrin and fibronectin. During aging, reduced responsiveness to FGF diminishes satellite cell self-renewal, leading to impaired skeletal muscle regeneration and depletion of satellite cells. Mislocalization of ß1-integrin, reductions in fibronectin, and alterations in heparan sulfate content all contribute to reduced FGF responsiveness in satellite cells. How these cell surface proteins regulate satellite cell self-renewal is incompletely understood. Here we summarize the current knowledge, highlighting the role(s) for FGF signaling in skeletal muscle regeneration, satellite cell behavior, and age-induced muscle wasting.

show abstract

Skeletal muscle: A review of molecular structure and function, in health and disease

Mukund

Subramaniam

2019

WIREs Mechanisms of Disease

306

253

View full text Add to dashboard Cite

Decades of research in skeletal muscle physiology have provided multiscale insights into the structural and functional complexity of this important anatomical tissue, designed to accomplish the task of generating contraction, force and movement. Skeletal muscle can be viewed as a biomechanical device with various interacting components including the autonomic nerves for impulse transmission, vasculature for efficient oxygenation, and embedded regulatory and metabolic machinery for maintaining cellular homeostasis. The “omics” revolution has propelled a new era in muscle research, allowing us to discern minute details of molecular cross‐talk required for effective coordination between the myriad interacting components for efficient muscle function. The objective of this review is to provide a systems‐level, comprehensive mapping the molecular mechanisms underlying skeletal muscle structure and function, in health and disease. We begin this review with a focus on molecular mechanisms underlying muscle tissue development (myogenesis), with an emphasis on satellite cells and muscle regeneration. We next review the molecular structure and mechanisms underlying the many structural components of the muscle: neuromuscular junction, sarcomere, cytoskeleton, extracellular matrix, and vasculature surrounding muscle. We highlight aberrant molecular mechanisms and their possible clinical or pathophysiological relevance. We particularly emphasize the impact of environmental stressors (inflammation and oxidative stress) in contributing to muscle pathophysiology including atrophy, hypertrophy, and fibrosis. This article is categorized under: Physiology > Mammalian Physiology in Health and Disease Developmental Biology > Developmental Processes in Health and Disease Models of Systems Properties and Processes > Cellular Models

show abstract

STAT3 Regulates Self-Renewal of Adult Muscle Satellite Cells during Injury-Induced Muscle Regeneration

Cited by 50 publications

References 67 publications

STAT3 in Skeletal Muscle Function and Disorders

STAT3 in Skeletal Muscle Function and Disorders

Regulation of skeletal muscle stem cells by fibroblast growth factors

Skeletal muscle: A review of molecular structure and function, in health and disease

Contact Info

Product

Resources

About