scholarly journals Matrix elasticity in vitro controls muscle stem cell fate in vivo

2010 ◽  
Vol 1 (5) ◽  
pp. 38 ◽  
Author(s):  
Matthew Raab ◽  
Jae-Won Shin ◽  
Dennis E Discher
Keyword(s):  
Stem Cell ◽  
Cell Fate ◽  
Muscle Stem Cell ◽  
Stem Cell Fate ◽  
Matrix Elasticity

scholarly journals Arginine Methylation by PRMT1 Regulates Muscle Stem Cell Fate

2016 ◽  
Vol 37 (3) ◽  
Author(s):  
Roméo Sébastien Blanc ◽  
Gillian Vogel ◽  
Xing Li ◽  
Zhenbao Yu ◽  
Shawn Li ◽  
...  
Keyword(s):  
Stem Cell ◽  
Cell Fate ◽  
Muscle Regeneration ◽  
Myogenic Differentiation ◽  
Arginine Methylation ◽  
Muscle Stem Cell ◽  
Stem Cell Fate ◽  
Protein Arginine Methyltransferase 1

ABSTRACT Quiescent muscle stem cells (MSCs) become activated in response to skeletal muscle injury to initiate regeneration. Activated MSCs proliferate and differentiate to repair damaged fibers or self-renew to maintain the pool and ensure future regeneration. The balance between self-renewal, proliferation, and differentiation is a tightly regulated process controlled by a genetic cascade involving determinant transcription factors such as Pax7, Myf5, MyoD, and MyoG. Recently, there have been several reports about the role of arginine methylation as a requirement for epigenetically mediated control of muscle regeneration. Here we report that the protein arginine methyltransferase 1 (PRMT1) is expressed in MSCs and that conditional ablation of PRMT1 in MSCs using Pax7CreERT2 causes impairment of muscle regeneration. Importantly, PRMT1-deficient MSCs have enhanced cell proliferation after injury but are unable to terminate the myogenic differentiation program, leading to regeneration failure. We identify the coactivator of Six1, Eya1, as a substrate of PRMT1. We show that PRMT1 methylates Eya1 in vitro and that loss of PRMT1 function in vivo prevents Eya1 methylation. Moreover, we observe that PRMT1-deficient MSCs have reduced expression of Eya1/Six1 target MyoD due to disruption of Eya1 recruitment at the MyoD promoter and subsequent Eya1-mediated coactivation. These findings suggest that arginine methylation by PRMT1 regulates muscle stem cell fate through the Eya1/Six1/MyoD axis.

Constructing stem cell microenvironments using bioengineering approaches

2013 ◽  
Vol 45 (23) ◽  
pp. 1123-1135 ◽  
Author(s):  
David A. Brafman
Keyword(s):  
Stem Cells ◽  
Stem Cell ◽  
Cell Fate ◽  
Disease Modeling ◽  
Mechanical Stimuli ◽  
Culture Methods ◽  
Stem Cell Fate ◽  
And Function

Within the adult organism, stem cells reside in defined anatomical microenvironments called niches. These architecturally diverse microenvironments serve to balance stem cell self-renewal and differentiation. Proper regulation of this balance is instrumental to tissue repair and homeostasis, and any imbalance can potentially lead to diseases such as cancer. Within each of these microenvironments, a myriad of chemical and physical stimuli interact in a complex (synergistic or antagonistic) manner to tightly regulate stem cell fate. The in vitro replication of these in vivo microenvironments will be necessary for the application of stem cells for disease modeling, drug discovery, and regenerative medicine purposes. However, traditional reductionist approaches have only led to the generation of cell culture methods that poorly recapitulate the in vivo microenvironment. To that end, novel engineering and systems biology approaches have allowed for the investigation of the biological and mechanical stimuli that govern stem cell fate. In this review, the application of these technologies for the dissection of stem cell microenvironments will be analyzed. Moreover, the use of these engineering approaches to construct in vitro stem cell microenvironments that precisely control stem cell fate and function will be reviewed. Finally, the emerging trend of using high-throughput, combinatorial methods for the stepwise engineering of stem cell microenvironments will be explored.

scholarly journals Synthetic Extracellular Microenvironment for Modulating Stem Cell Behaviors

2015 ◽  
Vol 10s1 ◽  
pp. BMI.S20057 ◽  
Author(s):  
Prafulla Chandra ◽  
Sang Jin Lee
Keyword(s):  
Stem Cells ◽  
Stem Cell ◽  
Cell Fate ◽  
Bioactive Molecules ◽  
Stem Cell Fate ◽  
Cell Behaviors ◽  
Extracellular Microenvironment ◽  
Promising Source

The innate ability of stem cells to self-renew and differentiate into multiple cell types makes them a promising source for tissue engineering and regenerative medicine applications. Their capacity for self-renewal and differentiation is largely influenced by the combination of physical, chemical, and biological signals found in the stem cell niche, both temporally and spatially. Embryonic and adult stem cells are potentially useful for cell-based approaches; however, regulating stem cell behavior remains a major challenge in their clinical use. Most of the current approaches for controlling stem cell fate do not fully address all of the complex signaling pathways that drive stem cell behaviors in their natural microenvironments. To overcome this limitation, a new generation of biomaterials is being developed for use as three-dimensional synthetic microenvironments that can mimic the regulatory characteristics of natural extracellular matrix (ECM) proteins and ECM-bound growth factors. These synthetic microenvironments are currently being investigated as a substrate with surface immobilization and controlled release of bioactive molecules to direct the stem cell fate in vitro, as a tissue template to guide and improve the neo-tissue formation both in vitro and in vivo, and as a delivery vehicle for cell therapy in vivo. The continued advancement of such an intelligent biomaterial system as the synthetic extracellular microenvironment holds the promise of improved therapies for numerous debilitating medical conditions for which no satisfactory cure exists today.

Analysis of Muscle Stem Cell Fate Through Modulation of AMPK Activity

2018 ◽  
pp. 539-549
Author(s):  
Marine Theret ◽  
Linda Gsaier ◽  
Sabrina Ben Larbi ◽  
Michèle Weiss-Gayet ◽  
Rémi Mounier
Keyword(s):  
Stem Cell ◽  
Cell Fate ◽  
Muscle Stem Cell ◽  
Stem Cell Fate ◽  
Ampk Activity

scholarly journals Regulation and Directing Stem Cell Fate by Tissue Engineering Functional Microenvironments: Scaffold Physical and Chemical Cues

2019 ◽  
Vol 2019 ◽  
pp. 1-16 ◽  
Author(s):  
Fei Xing ◽  
Lang Li ◽  
Changchun Zhou ◽  
Cheng Long ◽  
Lina Wu ◽  
...  
Keyword(s):  
Tissue Engineering ◽  
Stem Cells ◽  
Stem Cell ◽  
Growth Factors ◽  
Cell Fate ◽  
Chemical Cues ◽  
Physical Factors ◽  
Stem Cell Fate ◽  
Physical And Chemical

It is well known that stem cells reside within tissue engineering functional microenvironments that physically localize them and direct their stem cell fate. Recent efforts in the development of more complex and engineered scaffold technologies, together with new understanding of stem cell behavior in vitro, have provided a new impetus to study regulation and directing stem cell fate. A variety of tissue engineering technologies have been developed to regulate the fate of stem cells. Traditional methods to change the fate of stem cells are adding growth factors or some signaling pathways. In recent years, many studies have revealed that the geometrical microenvironment played an essential role in regulating the fate of stem cells, and the physical factors of scaffolds including mechanical properties, pore sizes, porosity, surface stiffness, three-dimensional structures, and mechanical stimulation may affect the fate of stem cells. Chemical factors such as cell-adhesive ligands and exogenous growth factors would also regulate the fate of stem cells. Understanding how these physical and chemical cues affect the fate of stem cells is essential for building more complex and controlled scaffolds for directing stem cell fate.

Increased Wnt Signaling During Aging Alters Muscle Stem Cell Fate and Increases Fibrosis

Science ◽  
2007 ◽  
Vol 317 (5839) ◽  
pp. 807-810 ◽  
Author(s):  
A. S. Brack ◽  
M. J. Conboy ◽  
S. Roy ◽  
M. Lee ◽  
C. J. Kuo ◽  
...  
Keyword(s):  
Stem Cell ◽  
Wnt Signaling ◽  
Cell Fate ◽  
Muscle Stem Cell ◽  
Stem Cell Fate
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