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  1. Article ; Online: Signaling pathways regulating the fate of fibro/adipogenic progenitors (FAPs) in skeletal muscle regeneration and disease

    Giuliani, Giulio / Rosina, Marco / Reggio, Alessio

    The FEBS Journal. 2022 Nov., v. 289, no. 21 p.6484-6517

    2022  

    Abstract: The characterization of fibro/adipogenic progenitor cells (FAPs) in the skeletal muscle has contributed to modify the monocentric view of muscle regeneration beyond muscle satellite cells (MuSCs). Now, we are aware that each population of the muscle ... ...

    Abstract The characterization of fibro/adipogenic progenitor cells (FAPs) in the skeletal muscle has contributed to modify the monocentric view of muscle regeneration beyond muscle satellite cells (MuSCs). Now, we are aware that each population of the muscle niche plays a critical role in modulating homeostasis and regeneration. In the healthy muscle, FAPs contribute to maintain tissue homeostasis and assist MuSCs to cope with limited insults. Here, FAPs sense and integrate niche signals that keep in check their differentiation potential. The disruption of these niche cues leads to FAP differentiation into adipocytes and fibroblasts, both detrimental hallmarks of a large variety of muscle wasting diseases. FAP biology is still in its infancy, and current efforts are focused on the understanding of the molecular circuits governing their double‐edged behavior. The present review offers a detailed overview of the pathways and metabolic routes that can be modulated to halt and redirect their fibro/adipogenic potential while favoring their supportive role in muscle regeneration. Finally, we discuss on how single‐cell technologies have contributed to resolve FAP transitional states with distinctive roles in muscle regeneration and myopathies.
    Keywords adipocytes ; fibroblasts ; homeostasis ; muscle development ; muscles ; skeletal muscle
    Language English
    Dates of publication 2022-11
    Size p. 6484-6517.
    Publishing place John Wiley & Sons, Ltd
    Document type Article ; Online
    Note REVIEW
    ZDB-ID 2173655-8
    ISSN 1742-4658 ; 1742-464X
    ISSN (online) 1742-4658
    ISSN 1742-464X
    DOI 10.1111/febs.16080
    Database NAL-Catalogue (AGRICOLA)

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  2. Article ; Online: Signaling pathways regulating the fate of fibro/adipogenic progenitors (FAPs) in skeletal muscle regeneration and disease.

    Giuliani, Giulio / Rosina, Marco / Reggio, Alessio

    The FEBS journal

    2021  Volume 289, Issue 21, Page(s) 6484–6517

    Abstract: The characterization of fibro/adipogenic progenitor cells (FAPs) in the skeletal muscle has contributed to modify the monocentric view of muscle regeneration beyond muscle satellite cells (MuSCs). Now, we are aware that each population of the muscle ... ...

    Abstract The characterization of fibro/adipogenic progenitor cells (FAPs) in the skeletal muscle has contributed to modify the monocentric view of muscle regeneration beyond muscle satellite cells (MuSCs). Now, we are aware that each population of the muscle niche plays a critical role in modulating homeostasis and regeneration. In the healthy muscle, FAPs contribute to maintain tissue homeostasis and assist MuSCs to cope with limited insults. Here, FAPs sense and integrate niche signals that keep in check their differentiation potential. The disruption of these niche cues leads to FAP differentiation into adipocytes and fibroblasts, both detrimental hallmarks of a large variety of muscle wasting diseases. FAP biology is still in its infancy, and current efforts are focused on the understanding of the molecular circuits governing their double-edged behavior. The present review offers a detailed overview of the pathways and metabolic routes that can be modulated to halt and redirect their fibro/adipogenic potential while favoring their supportive role in muscle regeneration. Finally, we discuss on how single-cell technologies have contributed to resolve FAP transitional states with distinctive roles in muscle regeneration and myopathies.
    MeSH term(s) Adipogenesis ; Adipocytes/metabolism ; Cell Differentiation ; Signal Transduction ; Muscle, Skeletal/metabolism ; Regeneration/genetics
    Language English
    Publishing date 2021-07-06
    Publishing country England
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't
    ZDB-ID 2173655-8
    ISSN 1742-4658 ; 1742-464X
    ISSN (online) 1742-4658
    ISSN 1742-464X
    DOI 10.1111/febs.16080
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    In stock of ZB MED Cologne/Königswinter

    Zs.A 260: Show issues Location:
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  3. Article: Endurance exercise has a negative impact on the onset of SOD1-G93A ALS in female mice and affects the entire skeletal muscle-motor neuron axis.

    Scaricamazza, Silvia / Nesci, Valentina / Salvatori, Illari / Fenili, Gianmarco / Rosina, Marco / Gloriani, Michela / Paronetto, Maria Paola / Madaro, Luca / Ferri, Alberto / Valle, Cristiana

    Frontiers in pharmacology

    2024  Volume 15, Page(s) 1360099

    Abstract: Background: Amyotrophic lateral sclerosis (ALS) is a fatal neuromuscular disease characterized by the degeneration of motor neurons that leads to muscle wasting and atrophy. Epidemiological and experimental evidence suggests a causal relationship ... ...

    Abstract Background: Amyotrophic lateral sclerosis (ALS) is a fatal neuromuscular disease characterized by the degeneration of motor neurons that leads to muscle wasting and atrophy. Epidemiological and experimental evidence suggests a causal relationship between ALS and physical activity (PA). However, the impact of PA on motor neuron loss and sarcopenia is still debated, probably because of the heterogeneity and intensities of the proposed exercises. With this study, we aimed to clarify the effect of intense endurance exercise on the onset and progression of ALS in the SOD1-G93A mouse model.
    Methods: We randomly selected four groups of twelve 35-day-old female mice. SOD1-G93A and WT mice underwent intense endurance training on a motorized treadmill for 8 weeks, 5 days a week. During the training, we measured muscle strength, weight, and motor skills and compared them with the corresponding sedentary groups to define the disease onset. At the end of the eighth week, we analyzed the skeletal muscle-motor neuron axis by histological and molecular techniques.
    Results: Intense endurance exercise anticipates the onset of the disease by 1 week (age of the onset: trained SOD1-G93A = 63.17 ± 2.25 days old; sedentary SOD1-G93A = 70.75 ± 2.45 days old). In SOD1-G93A mice, intense endurance exercise hastens the muscular switch to a more oxidative phenotype and worsens the denervation process by dismantling neuromuscular junctions in the tibialis anterior, enhancing the Wallerian degeneration in the sciatic nerve, and promoting motor neuron loss in the spinal cord. The training exacerbates neuroinflammation, causing immune cell infiltration in the sciatic nerve and a faster activation of astrocytes and microglia in the spinal cord.
    Conclusion: Intense endurance exercise, acting on skeletal muscles, worsens the pathological hallmarks of ALS, such as denervation and neuroinflammation, brings the onset forward, and accelerates the progression of the disease. Our findings show the potentiality of skeletal muscle as a target for both prognostic and therapeutic strategies; the preservation of skeletal muscle health by specific intervention could counteract the dying-back process and protect motor neurons from death. The physiological characteristics and accessibility of skeletal muscle further enhance its appeal as a therapeutic target.
    Language English
    Publishing date 2024-03-25
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2587355-6
    ISSN 1663-9812
    ISSN 1663-9812
    DOI 10.3389/fphar.2024.1360099
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  4. Article: Revisited role of TRAF2 and TRAF2 C-terminal domain in endoplasmic reticulum stress-induced autophagy in HAP1 leukemia cells

    Palumbo, Camilla / Mecchia, Alice / Bocedi, Alessio / Aquilano, Katia / Lettieri-Barbato, Daniele / Rosina, Marco / Di Venere, Almerinda / Rodolfo, Carlo / Caccuri, Anna Maria

    international journal of biochemistry & cell biology. 2022 Apr., v. 145

    2022  

    Abstract: The scaffold protein Tumor Necrosis Factor Receptor-Associated Factor 2 (TRAF2) has been reported to play a key role in the endoplasmic reticulum (ER) stress-induced activation of c-Jun N-terminal Kinase (JNK) and hence autophagy. Autophagy is a highly ... ...

    Abstract The scaffold protein Tumor Necrosis Factor Receptor-Associated Factor 2 (TRAF2) has been reported to play a key role in the endoplasmic reticulum (ER) stress-induced activation of c-Jun N-terminal Kinase (JNK) and hence autophagy. Autophagy is a highly conserved catabolic process, whose dysregulation is involved in the pathogenesis of various human diseases, including cancer. We investigated the involvement of TRAF2 in autophagy regulation in the human leukemic HAP1 cell line, under both basal and ER stress conditions. In TRAF2-knockout HAP1 cell line (KO), the basal autophagic flux was higher than in the parental cell line (WT). Moreover, tunicamycin-induced ER stress stimulated JNK activation and autophagy both in WT and KO HAP1. On the other hand, re-expression of a TRAF2 C-terminal fragment (residues ,310–501), in a TRAF2-KO cellular background, rendered HAP1 cells unable to activate both JNK and autophagy upon ER stress induction. Of note, this apparent dominant negative effect of the C-terminal fragment was observed even in the absence of the endogenous, full-length TRAF2 molecule. Furthermore, the expression of the C-terminal fragment resulted in both protein kinase B (AKT) pathway activation and increased resistance to the toxic effects induced by prolonged ER stress conditions. These findings indicate that TRAF2 is dispensable for the activation of both JNK and autophagy in HAP1 cells, while the TRAF2 C-terminal domain may play an autonomous role in regulating the cellular response to ER stress.
    Keywords amino acid sequences ; autophagy ; catabolism ; cell lines ; endoplasmic reticulum ; humans ; leukemia ; mitogen-activated protein kinase ; pathogenesis ; scaffolding proteins ; toxicity ; tumor necrosis factors
    Language English
    Dates of publication 2022-04
    Publishing place Elsevier Ltd
    Document type Article
    ZDB-ID 1228429-4
    ISSN 1878-5875 ; 1357-2725
    ISSN (online) 1878-5875
    ISSN 1357-2725
    DOI 10.1016/j.biocel.2022.106193
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    In stock of ZB MED Cologne/Königswinter

    Zs.A 431: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
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  5. Article ; Online: Trimetazidine Improves Mitochondrial Dysfunction in SOD1

    Salvatori, Illari / Nesci, Valentina / Spalloni, Alida / Marabitti, Veronica / Muzzi, Maurizio / Zenuni, Henri / Scaricamazza, Silvia / Rosina, Marco / Fenili, Gianmarco / Goglia, Mariangela / Boffa, Laura / Massa, Roberto / Moreno, Sandra / Mercuri, Nicola Biagio / Nazio, Francesca / Longone, Patrizia / Ferri, Alberto / Valle, Cristiana

    International journal of molecular sciences

    2024  Volume 25, Issue 6

    Abstract: Amyotrophic Lateral Sclerosis (ALS) is considered the prototype of motor neuron disease, characterized by motor neuron loss and muscle waste. A well-established pathogenic hallmark of ALS is mitochondrial failure, leading to bioenergetic deficits. So far, ...

    Abstract Amyotrophic Lateral Sclerosis (ALS) is considered the prototype of motor neuron disease, characterized by motor neuron loss and muscle waste. A well-established pathogenic hallmark of ALS is mitochondrial failure, leading to bioenergetic deficits. So far, pharmacological interventions for the disease have proven ineffective. Trimetazidine (TMZ) is described as a metabolic modulator acting on different cellular pathways. Its efficacy in enhancing muscular and cardiovascular performance has been widely described, although its molecular target remains elusive. We addressed the molecular mechanisms underlying TMZ action on neuronal experimental paradigms. To this aim, we treated murine SOD1
    MeSH term(s) Mice ; Animals ; Humans ; Amyotrophic Lateral Sclerosis/metabolism ; Superoxide Dismutase-1/metabolism ; Trimetazidine/pharmacology ; Trimetazidine/therapeutic use ; Mice, Transgenic ; Leukocytes, Mononuclear/metabolism ; Superoxide Dismutase/metabolism ; Autophagy ; Mitochondrial Diseases ; Disease Models, Animal
    Chemical Substances Superoxide Dismutase-1 (EC 1.15.1.1) ; Trimetazidine (N9A0A0R9S8) ; Superoxide Dismutase (EC 1.15.1.1) ; SOD1 protein, human
    Language English
    Publishing date 2024-03-13
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms25063251
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  6. Article ; Online: FoxO1 localizes to mitochondria of adipose tissue and is affected by nutrient stress.

    Lettieri-Barbato, Daniele / Ioannilli, Laura / Aquilano, Katia / Ciccarone, Fabio / Rosina, Marco / Ciriolo, Maria Rosa

    Metabolism: clinical and experimental

    2019  Volume 95, Page(s) 84–92

    Abstract: Objective: Mitochondria play pivotal roles in orchestrating signaling pathways in order to guarantee metabolic homeostasis under different stimuli. It has been demonstrated that the mito-nuclear communication is fundamental for facing physiological and/ ... ...

    Abstract Objective: Mitochondria play pivotal roles in orchestrating signaling pathways in order to guarantee metabolic homeostasis under different stimuli. It has been demonstrated that the mito-nuclear communication is fundamental for facing physiological and/or stress-mediated cellular response through the activation of nuclear transcription factors. Here, we focused on the Forkhead box protein O1 (FoxO1) transcription factor that belongs to the FoxOs family proteins and is considered a "nutrients sensor" modulating the expression of nutrient-stress response genes.
    Methods: In vitro and in vivo experimental systems, including 3T3-L1 white, X-9 beige and T37i brown adipocytes and different fat depots from C57BL/6 mice were used. The mitochondrial localization of FoxO1 was demonstrated by western blot analysis, confocal microscopy and chromatin immunoprecipitation assay, after sub-cellular compartment isolation. RT-qPCR analysis was used to evaluate the expression of antioxidant and mitochondrial genes after modulation of FoxO1 activity/localization. Treatment with diverse reactive oxygen species (ROS) species/sources were performed and assessed by cytofluorimetric analysis.
    Results: We demonstrated that FoxO1 not exclusively localizes to cytosol and nucleus of adipocytes but also to mitochondria where it binds to mitochondrial DNA. We also proved that mitochondrial FoxO1 is phosphorylated upon normal feeding condition. Mitochondrial FoxO1 responds to starvation leaving mitochondrial compartment by ROS-mediated activation of the mitochondrial phosphatase PTPMT1. Indeed, FoxO1 de-phosphorylation and mito-to-nucleus shuttling was observed under starvation. Moreover, we provided evidence that ROS species/sources are able to differently modulate the mitochondrial localization of FoxO1.
    Conclusion: The ability to localize at different cell compartments, including mitochondria, highlights a different layer of regulation of FoxO1 necessary for assuring a fast and efficient nutrient-stress response in white/beige adipose tissue. FoxO1 could be thus endorsed in the list of transcription factors involved in the mito-nuclear communication where ROS can act as upstream signals.
    MeSH term(s) 3T3 Cells ; Adipocytes/metabolism ; Adipose Tissue/metabolism ; Animals ; Antioxidants/metabolism ; Caloric Restriction ; Cell Nucleus/metabolism ; Cytosol/metabolism ; Forkhead Box Protein O1/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Mitochondria/metabolism ; PTEN Phosphohydrolase/metabolism ; Phosphorylation ; Reactive Oxygen Species/metabolism
    Chemical Substances Antioxidants ; Forkhead Box Protein O1 ; Foxo1 protein, mouse ; Reactive Oxygen Species ; Ptpmt1 protein, mouse (EC 3.1.3.27) ; PTEN Phosphohydrolase (EC 3.1.3.67)
    Language English
    Publishing date 2019-04-08
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 80230-x
    ISSN 1532-8600 ; 0026-0495
    ISSN (online) 1532-8600
    ISSN 0026-0495
    DOI 10.1016/j.metabol.2019.04.006
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    In stock of ZB MED Cologne/Königswinter

    Uc I Zs.316: Show issues Location:
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    bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
    ab Jg. 2022: Lesesaal (EG)

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  7. Article ; Online: Revisited role of TRAF2 and TRAF2 C-terminal domain in endoplasmic reticulum stress-induced autophagy in HAP1 leukemia cells.

    Palumbo, Camilla / Mecchia, Alice / Bocedi, Alessio / Aquilano, Katia / Lettieri-Barbato, Daniele / Rosina, Marco / Di Venere, Almerinda / Rodolfo, Carlo / Caccuri, Anna Maria

    The international journal of biochemistry & cell biology

    2022  Volume 145, Page(s) 106193

    Abstract: The scaffold protein Tumor Necrosis Factor Receptor-Associated Factor 2 (TRAF2) has been reported to play a key role in the endoplasmic reticulum (ER) stress-induced activation of c-Jun N-terminal Kinase (JNK) and hence autophagy. Autophagy is a highly ... ...

    Abstract The scaffold protein Tumor Necrosis Factor Receptor-Associated Factor 2 (TRAF2) has been reported to play a key role in the endoplasmic reticulum (ER) stress-induced activation of c-Jun N-terminal Kinase (JNK) and hence autophagy. Autophagy is a highly conserved catabolic process, whose dysregulation is involved in the pathogenesis of various human diseases, including cancer. We investigated the involvement of TRAF2 in autophagy regulation in the human leukemic HAP1 cell line, under both basal and ER stress conditions. In TRAF2-knockout HAP1 cell line (KO), the basal autophagic flux was higher than in the parental cell line (WT). Moreover, tunicamycin-induced ER stress stimulated JNK activation and autophagy both in WT and KO HAP1. On the other hand, re-expression of a TRAF2 C-terminal fragment (residues ,310-501), in a TRAF2-KO cellular background, rendered HAP1 cells unable to activate both JNK and autophagy upon ER stress induction. Of note, this apparent dominant negative effect of the C-terminal fragment was observed even in the absence of the endogenous, full-length TRAF2 molecule. Furthermore, the expression of the C-terminal fragment resulted in both protein kinase B (AKT) pathway activation and increased resistance to the toxic effects induced by prolonged ER stress conditions. These findings indicate that TRAF2 is dispensable for the activation of both JNK and autophagy in HAP1 cells, while the TRAF2 C-terminal domain may play an autonomous role in regulating the cellular response to ER stress.
    MeSH term(s) Apoptosis ; Autophagy/genetics ; Endoplasmic Reticulum Stress/genetics ; Humans ; JNK Mitogen-Activated Protein Kinases/metabolism ; Leukemia/genetics ; Nerve Tissue Proteins/metabolism ; Signal Transduction ; TNF Receptor-Associated Factor 2/genetics ; TNF Receptor-Associated Factor 2/metabolism ; TNF Receptor-Associated Factor 2/pharmacology ; Ubiquitin-Protein Ligases/metabolism
    Chemical Substances HAP1 protein, human ; Nerve Tissue Proteins ; PSMD2 protein, human ; TNF Receptor-Associated Factor 2 ; Ubiquitin-Protein Ligases (EC 2.3.2.27) ; JNK Mitogen-Activated Protein Kinases (EC 2.7.11.24)
    Language English
    Publishing date 2022-03-05
    Publishing country Netherlands
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1228429-4
    ISSN 1878-5875 ; 1357-2725
    ISSN (online) 1878-5875
    ISSN 1357-2725
    DOI 10.1016/j.biocel.2022.106193
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    In stock of ZB MED Cologne/Königswinter

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    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

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  8. Article ; Online: High-Dimensional Single-Cell Quantitative Profiling of Skeletal Muscle Cell Population Dynamics during Regeneration.

    Petrilli, Lucia Lisa / Spada, Filomena / Palma, Alessandro / Reggio, Alessio / Rosina, Marco / Gargioli, Cesare / Castagnoli, Luisa / Fuoco, Claudia / Cesareni, Gianni

    Cells

    2020  Volume 9, Issue 7

    Abstract: The interstitial space surrounding the skeletal muscle fibers is populated by a variety of mononuclear cell types. Upon acute or chronic insult, these cell populations become activated and initiate finely-orchestrated crosstalk that promotes myofiber ... ...

    Abstract The interstitial space surrounding the skeletal muscle fibers is populated by a variety of mononuclear cell types. Upon acute or chronic insult, these cell populations become activated and initiate finely-orchestrated crosstalk that promotes myofiber repair and regeneration. Mass cytometry is a powerful and highly multiplexed technique for profiling single-cells. Herein, it was used to dissect the dynamics of cell populations in the skeletal muscle in physiological and pathological conditions. Here, we characterized an antibody panel that could be used to identify most of the cell populations in the muscle interstitial space. By exploiting the mass cytometry resolution, we provided a comprehensive picture of the dynamics of the major cell populations that sensed and responded to acute damage in wild type mice and in a mouse model of Duchenne muscular dystrophy. In addition, we revealed the intrinsic heterogeneity of many of these cell populations.
    MeSH term(s) Animals ; Cardiotoxins ; Cell Count ; Disease Models, Animal ; Mice, Inbred C57BL ; Mice, Inbred mdx ; Muscle, Skeletal/pathology ; Muscular Dystrophy, Duchenne/pathology ; Regeneration ; Single-Cell Analysis/methods
    Chemical Substances Cardiotoxins
    Language English
    Publishing date 2020-07-18
    Publishing country Switzerland
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2661518-6
    ISSN 2073-4409 ; 2073-4409
    ISSN (online) 2073-4409
    ISSN 2073-4409
    DOI 10.3390/cells9071723
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  9. Article: Metformin Delays Satellite Cell Activation and Maintains Quiescence.

    Pavlidou, Theodora / Marinkovic, Milica / Rosina, Marco / Fuoco, Claudia / Vumbaca, Simone / Gargioli, Cesare / Castagnoli, Luisa / Cesareni, Gianni

    Stem cells international

    2019  Volume 2019, Page(s) 5980465

    Abstract: The regeneration of the muscle tissue relies on the capacity of the satellite stem cell (SC) population to exit quiescence, divide asymmetrically, proliferate, and differentiate. In age-related muscle atrophy (sarcopenia) and several dystrophies, ... ...

    Abstract The regeneration of the muscle tissue relies on the capacity of the satellite stem cell (SC) population to exit quiescence, divide asymmetrically, proliferate, and differentiate. In age-related muscle atrophy (sarcopenia) and several dystrophies, regeneration cannot compensate for the loss of muscle tissue. These disorders are associated with the depletion of the satellite cell pool or with the loss of satellite cell functionality. Recently, the establishment and maintenance of quiescence in satellite cells have been linked to their metabolic state. In this work, we aimed to modulate metabolism in order to preserve the satellite cell pool. We made use of metformin, a calorie restriction mimicking drug, to ask whether metformin has an effect on quiescence, proliferation, and differentiation of satellite cells. We report that satellite cells, when treated with metformin
    Language English
    Publishing date 2019-04-24
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2573856-2
    ISSN 1687-9678 ; 1687-966X
    ISSN (online) 1687-9678
    ISSN 1687-966X
    DOI 10.1155/2019/5980465
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: The immunosuppressant drug azathioprine restrains adipogenesis of muscle Fibro/Adipogenic Progenitors from dystrophic mice by affecting AKT signaling.

    Reggio, Alessio / Spada, Filomena / Rosina, Marco / Massacci, Giorgia / Zuccotti, Alessandro / Fuoco, Claudia / Gargioli, Cesare / Castagnoli, Luisa / Cesareni, Gianni

    Scientific reports

    2019  Volume 9, Issue 1, Page(s) 4360

    Abstract: Fibro/Adipogenic Progenitors (FAPs) define a stem cell population playing a pro-regenerative role after muscle damage. When removed from their natural niche, FAPs readily differentiate into adipocytes or fibroblasts. This digressive differentiation ... ...

    Abstract Fibro/Adipogenic Progenitors (FAPs) define a stem cell population playing a pro-regenerative role after muscle damage. When removed from their natural niche, FAPs readily differentiate into adipocytes or fibroblasts. This digressive differentiation potential, which is kept under tight control in the healthy muscle niche, contributes to fat and scar infiltrations in degenerative myopathies, such as in Duchenne Muscular Dystrophy (DMD). Controlling FAP differentiation by means of small molecules may contribute to delay the adverse consequences of the progressive pathological degeneration while offering, at the same time, a wider temporal window for gene therapy and cell-based strategies. In a high content phenotypic screening, we identified the immunosuppressant, azathioprine (AZA) as a negative modulator of FAP adipogenesis. We show here that AZA negatively affects the adipogenic propensity of FAPs purified from wild type and mdx mice by impairing the expression of the master adipogenic regulator, peroxisome proliferator-activated receptor γ (PPARγ). We show that this inhibition correlates with a decline in the activation of the AKT-mTOR axis, the main pathway that transduces the pro-adipogenic stimulus triggered by insulin. In addition, AZA exerts a cytostatic effect that has a negative impact on the mitotic clonal process that is required for the terminal differentiation of the preadipocyte-committed cells.
    MeSH term(s) Adipogenesis/drug effects ; Animals ; Azathioprine/pharmacology ; Cell Differentiation/drug effects ; Cells, Cultured ; Disease Models, Animal ; Fibroblasts/drug effects ; Fibroblasts/metabolism ; Immunosuppressive Agents/pharmacology ; Mice ; Mice, Inbred mdx ; Models, Biological ; Muscular Dystrophy, Duchenne ; Myoblasts, Skeletal/drug effects ; Myoblasts, Skeletal/metabolism ; PPAR gamma ; Proto-Oncogene Proteins c-akt/metabolism ; Signal Transduction/drug effects ; Stem Cells/drug effects ; Stem Cells/metabolism ; TOR Serine-Threonine Kinases/metabolism
    Chemical Substances Immunosuppressive Agents ; PPAR gamma ; TOR Serine-Threonine Kinases (EC 2.7.1.1) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; Azathioprine (MRK240IY2L)
    Language English
    Publishing date 2019-03-13
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2615211-3
    ISSN 2045-2322 ; 2045-2322
    ISSN (online) 2045-2322
    ISSN 2045-2322
    DOI 10.1038/s41598-019-39538-y
    Database MEDical Literature Analysis and Retrieval System OnLINE

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