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Autonomous extracellular matrix remodeling controls a progressive adaptation in muscle stem cell regenerative capacity during development

ABSTRACT: Muscle stem cells (MuSC) exhibit distinct behaviors during successive phases of developmental myogenesis. However, how their transition to adulthood is regulated is poorly understood. Here we show that fetal MuSC resist progenitor specification and exhibit altered division dynamics, intrinsic features that are progressively lost postnatally. Following transplantation, fetal MuSC more efficiently expand and contribute to muscle repair. Conversely, the efficiency of niche colonization increases in adulthood, indicating a balance between muscle growth and stem cell pool repopulation. Gene expression profiling identified several extracellular matrix (ECM) molecules preferentially expressed in fetal MuSC, including tenascin-C, fibronectin and collagen VI. Loss-of-function experiments confirmed their essential and stage-specific role in regulating MuSC function. Finally, fetal-derived paracrine factors were able to enhance adult MuSC regenerative potential. Together, these findings demonstrate that MuSC change the way in which they remodel their microenvironment to direct stem cell behavior in support of the unique demands of muscle development or repair.

ORGANISM(S): Mus musculus

PROVIDER: GSE76989 | GEO | 2016/01/20

SECONDARY ACCESSION(S): PRJNA309185

REPOSITORIES: GEO

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Autonomous extracellular matrix remodeling controls a progressive adaptation in muscle stem cell regenerative capacity during development

Project description:Muscle stem cells (MuSC) exhibit distinct behaviors during successive phases of developmental myogenesis. However, how their transition to adulthood is regulated is poorly understood. Here we show that fetal MuSC resist progenitor specification and exhibit altered division dynamics, intrinsic features that are progressively lost postnatally. Following transplantation, fetal MuSC more efficiently expand and contribute to muscle repair. Conversely, the efficiency of niche colonization increases in adulthood, indicating a balance between muscle growth and stem cell pool repopulation. Gene expression profiling identified several extracellular matrix (ECM) molecules preferentially expressed in fetal MuSC, including tenascin-C, fibronectin and collagen VI. Loss-of-function experiments confirmed their essential and stage-specific role in regulating MuSC function. Finally, fetal-derived paracrine factors were able to enhance adult MuSC regenerative potential. Together, these findings demonstrate that MuSC change the way in which they remodel their microenvironment to direct stem cell behavior in support of the unique demands of muscle development or repair. MuSCs were isolated through fluorescent-activate cell sorting usinf alpha7-integirn and CD34 as markers to identify the cell population. Total mRNA was then isolated, and samples at different developmental times were compared.

2016-01-20 | E-GEOD-76989 | biostudies-arrayexpress

Elevated Extracellular Purine Nucleotides Impair Muscle Regeneration in Diabetic Mice by Suppressing Early Activation of Muscle Satellite Cells

Project description:Chronic diabetic patients often exhibit defective tissue repair. Similarly, injury-induced muscle regeneration was also found to be defective in diabetic mice. However, the underlying mechanisms remain obscure. Here, we found that quiescent muscle satellite cells (MuSC) from db/db diabetic mice, a mouse model for obesity-induced type 2 diabetes, failed to re-enter the cell cycle upon activation in vivo but not in culture, suggesting the involvement of certain niche factors. Elevated extracellular AMP (eAMP) and adenosine (eAdo) were detected in both muscle tissues and blood of diabetic patients and mice. Unexpectedly, we found that eAMP and eAdo potently inhibited cell cycle re-entry of MuSC, and consequently impaired injury-induced muscle regeneration. Mechanistically, we demonstrated that eAMP and eAdo impaired the functions of MuSC via a signaling axis of equilibrative Ado transporter (ENT)-Ado kinase (ADK)-AMPK, which in turn inhibited an mTORC1-dependent cell growth checkpoint and subsequent cell cycle re-entry. Moreover, eAdo also inhibited early activation of quiescent fibroadipogenic progenitors and human MuSC by the same mechanism. Importantly, treatment of db/db diabetic mice with an ADK inhibitor not only reduced plasma glucose level but also partially restored the regenerative functions of MuSC in vivo. Collectively, our study suggests that both ENT and ADK are promising therapeutic targets for the treatment of diabetes and for restoring the regenerative functions of tissue stem cells.

2022-05-28 | GSE175786 | GEO

Restoration of CPEB4 Prevents Muscle Stem Cell Senescence during Aging

Project description:Muscle stem cells (MuSCs) are required for muscle regeneration. In resting muscles, MuSCs are kept in quiescence. After injury, MuSCs undergo rapid activation, proliferation and differentiation to repair damaged muscles. Age-associated impairments in stem cell functions correlate with a decline in somatic tissue regeneration capacity during aging. However, the mechanisms underlying the molecular regulation of adult stem cell aging remain elusive. Here, we obtained quisecent MuSCs from young, old, geriatric mice for high resolution mass spectrometry Bruker timsTOF Pro. By comparison of young proteome to old MuSCs proteome or geriatric MuSC proteome, we identified the pathways that are differentially during aging.

2023-06-26 | PXD041614 | Pride

H3K27me3 CUT&Tag - Jmjd3-scKO, Utx-scKO, Tdt-Ctrl, IgG-His

Project description:Stem cells reside in specialized niches that play a critical role in modulating their fate. Supporting cells in the niche instruct fate changes to the stem cells through epigenetic enzymes that transduce cell signaling to modify gene expression. Recent studies showed that the innate immune response to muscle injury alters the muscle stem cell (MuSC) niche, it remains unknown how MuSC adapt to the modified milieu to mediate muscle repair. Here we show that the epigenetic enzyme JMJD3 coordinates MuSC adaptation to the regenerative niche in a non-cell autonomous manner where it modifies their extracellular matrix to integrate signaling that stimulates exit of quiescence. Genomics and transcriptomics approaches identified the hyaluronic acid (HA) synthesis enzyme Has2 as a key JMJD3 target gene that allows MuSCs to integrate signals from the regenerative niche. Overall, we identified a specific role for JMJD3 in regulating the expression of genes that allow MuSCs to adapt to the modified niche of regenerating muscle. We aim to determine the differential occupancy of histone H3 lysine 4 trimethyl mark muscle satellite stem cells isolated from JMJD3scKO, UTXscKO and Wild-type mice.

2022-08-04 | GSE186830 | GEO

H3K4me3 CUT&Tag - Jmjd3-scKO, Utx-scKO, Tdt-Ctrl, IgG-His

2022-08-04 | GSE186829 | GEO

Jmjd3-Lab UTX-Lab CUT&Tag

2022-08-04 | GSE186828 | GEO

Transcriptional profiling of embryonic skeletal muscle stem/progenitor cells

Project description:Muscle stem cells (MuSC) change molecular and functional properties during development. Using a transgenic Tg:Pax7-nGFP mice, we FACS-isolated MuSC from embryonic (E12.5) and foetal (E17.5) stages to understand the differences and similarities amongst the myogenic stem/progenitor populations. Pax7-nGFP+ cells were isolated by FACS from limb buds of E12.5 and E17.5 Tg:Pax7-nGFP embryos following enzymatic digestion. Affymetrix microarrays were performed on biological triplicates.

2013-11-08 | E-GEOD-52192 | biostudies-arrayexpress

Single-cell analysis of homeostatic and regenerative adult skeletal muscle stem cells

Project description:Skeletal muscle stem cells (MuSCs) ensure the formation and homeostasis of skeletal muscle and are responsible for its growth and repair processes. For repair to occur, MuSCs must exit from quiescence, abandon their niche and asymmetrically and symmetrically divide to reconstitute the stem cell pool and give rise to muscle progenitors, respectively. The transcriptomes of pooled MuSCs have provided a rich source of information for describing the genetic programs underlying distinct static cell states; however, bulk microarray and RNA-seq afford only averaged gene expression profiles, which blur the heterogeneity and developmental dynamics of asynchronous MuSC populations. The granularity required to identify distinct cell types, states, and their dynamics can be provided by single-cell analysis. We were able to compare the transcriptomes of thousands of MuSCs and primary myoblasts isolated from homeostatic or regenerating muscles by single-cell RNA- sequencing. Using computational approaches, we could reconstruct dynamic trajectories and place, in a pseudotemporal manner, the transcriptomes of individual MuSC within these trajectories. This approach allowed for the identification of distinct clusters of MuSCs and primary myoblasts with partially overlapping but distinct transcriptional signatures, as well as the description of metabolic pathways associated with defined MuSC states.

2019-03-08 | GSE126834 | GEO

Overloading mesenchymal progenitors (FAPs)

Project description:Skeletal muscle possesses the ability to adapt its size in response to milieus, which is called plasticity. Resistance training induces the increment of muscle mass called muscle hypertrophy. Muscle stem cells (MuSC; also known as muscle stem cells) function to supply new nuclei for myofiber during the overload in muscle. We found that Yap1 and Taz in mesenchymal progenitors (also called FAPs) are critical for MuSC proliferation in overloaded muscles. We hypothsize that Yap1/Taz-dependent mesenchymal progenitors derived factor induces MuSC proliferation. In order to identify such factors, RNA-seq of overloaded FAPs were performed.

2021-11-19 | GSE162827 | GEO

Overloading mesenchymal progenitors (FAPs)

Project description:Skeletal muscle possesses the ability to adapt its size in response to milieus, which is called plasticity. Resistance training induces the increment of muscle mass called muscle hypertrophy. Muscle stem cells (MuSC; also known as muscle stem cells) function to supply new nuclei for myofiber during the overload in muscle. We hypothesize that mesenchymal progenitors (also called FAPs) -derived factor induces MuSC proliferation. In order to identify such factors, RNA-seq of overloaded FAPs were performed.

2021-11-19 | GSE159082 | GEO

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