Browsing by Author "Contreras Saavedra, Osvaldo Isaías"

Now showing 1 - 18 of 18
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    ALS skeletal muscle shows enhanced TGF-β signaling, fibrosis and induction of fibro/adipogenic progenitor markers.
    (2017) Gonzalez, David; Contreras Saavedra, Osvaldo Isaías; Brandan, Enrique; Rebolledo López, Daniela Victoria; Espinoza, Juan Pablo; Zundert, Brigitte van
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    Cross-talk between TGF-β and PDGFRα signaling pathways regulates the fate of stromal fibro–adipogenic progenitors
    (2019) Contreras Saavedra, Osvaldo Isaías; Cruz Soca, Meilyn; Theret, Marine; Soliman, Hesham; Wei Tung, Lin; Groppa, Elena; Rossi, Fabio M.; Brandan, Enrique
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    Denervation-induced skeletal muscle fibrosis is mediated by CTGF/CCN2 independently of TGF-β
    (2019) Rebolledo, Daniela L.; González, David; Faundez Contreras, Jennifer; Contreras Saavedra, Osvaldo Isaías; Vio Lagos, Carlos P.; Murphy Ullrich, Joanne E.; Lipson, Kenneth E.; Brandan, Enrique; Rebolledo, Daniela L.; González, David; Faundez Contreras, Jennifer; Contreras Saavedra, Osvaldo Isaías; Vio Lagos, Carlos P.; Murphy Ullrich, Joanne E.; Lipson, Kenneth E.; Brandan, Enrique
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    Expression of CTGF/CCN2 in response to LPA is stimulated by fibrotic extracellular matrix via the integrin/FAK axis
    (2018) Riquelme Guzmán, Camilo; Contreras Saavedra, Osvaldo Isaías; Brandan, Enrique
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    Fibro/adipogenic progenitors safeguard themselves : a novel mechanism to reduce fibrosis is discovered.
    (2017) Contreras Saavedra, Osvaldo Isaías; Brandan, Enrique
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    First person – Osvaldo Contreras
    (2019) Contreras Saavedra, Osvaldo Isaías
    First Person is a series of interviews with the first authors of a selection of papers published in Journal of Cell Science, helping early-career researchers promote themselves alongside their papers. Osvaldo Contreras is first author on ‘Cross-talk between TGF-β and PDGFRα signaling pathways regulates the fate of stromal fibro–adipogenic progenitors’, published in JCS. Osvaldo is a postdoctoral scientist in the laboratory of Enrique Brandan at Departamento de Biología Celular y Molecular and Center for Aging and Regeneration (CARE-ChileUC), Facultad de Ciencias Biológicas, Pontificia Universidad Católica de Chile, Santiago, Chile, investigating skeletal muscle tissue-resident mesenchymal progenitors in health and disease.
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    Nilotinib impairs skeletal myogenesis by increasing myoblast proliferation.
    (2018) Contreras Saavedra, Osvaldo Isaías; Villarreal, M.; Brandan, Enrique
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    Origins, potency, and heterogeneity of skeletal muscle fibro-adipogenic progenitors—time for new definitions
    (2021) Contreras Saavedra, Osvaldo Isaías; Rossi, Fabio M.; Theret, Marine
    Abstract Striated muscle is a highly plastic and regenerative organ that regulates body movement, temperature, and metabolism—all the functions needed for an individual’s health and well-being. The muscle connective tissue’s main components are the extracellular matrix and its resident stromal cells, which continuously reshape it in embryonic development, homeostasis, and regeneration. Fibro-adipogenic progenitors are enigmatic and transformative muscle-resident interstitial cells with mesenchymal stem/stromal cell properties. They act as cellular sentinels and physiological hubs for adult muscle homeostasis and regeneration by shaping the microenvironment by secreting a complex cocktail of extracellular matrix components, diffusible cytokines, ligands, and immune-modulatory factors. Fibro-adipogenic progenitors are the lineage precursors of specialized cells, including activated fibroblasts, adipocytes, and osteogenic cells after injury. Here, we discuss current research gaps, potential druggable developments, and outstanding questions about fibro-adipogenic progenitor origins, potency, and heterogeneity. Finally, we took advantage of recent advances in single-cell technologies combined with lineage tracing to unify the diversity of stromal fibro-adipogenic progenitors. Thus, this compelling review provides new cellular and molecular insights in comprehending the origins, definitions, markers, fate, and plasticity of murine and human fibro-adipogenic progenitors in muscle development, homeostasis, regeneration, and repair.
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    RECK-Mediated beta 1-Integrin Regulation by TGF-beta 1 Is Critical for Wound Contraction in Mice
    (2015) Gutiérrez Pérez, Jaime Agustín; Droppelmann Rosas, Cristian Andrés; Contreras Saavedra, Osvaldo Isaías
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    RECK-Mediated β1-Integrin Regulation by TGF-β1 Is Critical for Wound Contraction in Mice.
    (2015) Gutiérrez Pérez, Jaime Agustín; Contreras Saavedra, Osvaldo Isaías; Droppelmann Rosas, Cristian Andrés; Brandan, Enrique; Takahashi, Chiaki
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    Role of mesenchymal fibro/adipogenic progenitors in homeostasis and disease : from signaling to fibrosis
    (2019) Contreras Saavedra, Osvaldo Isaías; Brandan, Enrique; Pontificia Universidad Católica de Chile. Facultad de Ciencias Biológicas
    Fibrosis, the dysregulated accumulation of connective tissue (CT), is a hallmark of multiple pathologies where inflammation is not fully resolved. The main components of the CT are the extracellular matrix (ECM) and its tissue-resident mesenchymal stromal cells (MSCs), which actively produce and remodel ECM during development, homeostasis, and disease. Fibrosis and/or fibro-fatty replacement of the functional tissue is a common feature of Duchenne Muscular Dystrophy (DMD), but it is also observed in neuromuscular diseases. It is generally accepted that these mesenchymal progenitor cells (MPCs) [hereafter referred to as fibro/adipogenic progenitors (FAPs)] are the progenitors of pathological myofibroblasts and adipocytes during muscular dystrophy and chronic muscle damage, but also important players for proper tissue regeneration. Their dysregulated activity during pathology impairs proper tissue repair. Our overall hypothesis is that efficient regeneration depends on a complex network of signaling interactions between multiple cell types leading to the proper coordination of their function. The best-known marker for FAPs is the receptor tyrosine kinase (RTK) plateletderived growth factor receptor alpha (PDGFRa). Several attempts to block the dysregulated RTK activity of PDGFRa in pathology have been successfully done, therefore, PDGFRa signaling emerges as a potential target against fibrosis. TGF-bmediated signaling pathways are commonly accepted to be fibrotic, to induce the proliferation of FAPs and myofibroblast differentiation from these precursors. TGF-b signaling and its ligands are augmented during DMD, and fibrosis in several tissues. Hence, TGF-b is a known driver of the fibrotic process. Here, we investigated the role of TGF-b signaling on PDGFRa expression and signaling, along with studying a functional cross-talk between PDGFRa and TGF-b in FAPs and MPCs. Canonical Wnt Tcf/Lef transcription factors are important players during development and controlling stem cell fate. Recently, the canonical Wnt signaling cascade emerged as a new system to study fibrosis in several tissues. Importantly, the role of Tcf/lef proteins in MPCs has not been studied yet. Additionally, whether TGF-b has an impact on Wnt signaling and/or may crosstalk through the regulation of these Wnt transcription factors has not been explored yet. In the present Ph.D. thesis, we focused on the TGF-b signaling pathway and its role in FAPs and MPCs. The main findings are; 1. MPCs are present in skeletal muscle under normal conditions and are increased in several models where muscle fibrosis and TGF-b are a hallmark. These Tcf7l2+ progenitors lie near macrophages mainly concentrated in dystrophic necrotic-regenerating foci. 2. We suggest that the historically named muscle CT fibroblasts isolated via pre-plating correspond to a phenotypically and biochemically FAPs-like population of adherent MPCs. These adherent cells respond in the same fashion to TGF-b signaling and the tyrosine kinase inhibitor Nilotinib as FAPs. 3. The role and/or cross-talk of TGF-b signaling in the regulation of PDGFRa expression and signaling in mesenchymal progenitors is described: i) PDGFRa expression is strongly reduced by TGF-b signaling in FAPs, Hic1+ MPs, skin fibroblasts, and two different MPs cell lines. ii) PDGFRa-mediated gene expression is altered during muscle regeneration in FAPs and after TGF-b1 treatment. iii) Pharmacological inhibition of PDGFRa impaired the TGF-b-mediated ECM remodeling and blocked the TGF-b1-induced migration of MPs. 4. the ubiquitin-proteasome system (UPS). Via Tcf7l2 pharmacological inhibition we suggest that Tcf7l2 plays a role in regulating FAPs survival and fate. Therefore, in this Ph.D. Thesis we studied and proposed that FAPs modulators and signaling governing pathways might be suitable for a novel therapeutic target for the treatment of MD, neurodegenerative diseases, non-malignant fibroproliferative disorders, and aging.Fibrosis, the dysregulated accumulation of connective tissue (CT), is a hallmark of multiple pathologies where inflammation is not fully resolved. The main components of the CT are the extracellular matrix (ECM) and its tissue-resident mesenchymal stromal cells (MSCs), which actively produce and remodel ECM during development, homeostasis, and disease. Fibrosis and/or fibro-fatty replacement of the functional tissue is a common feature of Duchenne Muscular Dystrophy (DMD), but it is also observed in neuromuscular diseases. It is generally accepted that these mesenchymal progenitor cells (MPCs) [hereafter referred to as fibro/adipogenic progenitors (FAPs)] are the progenitors of pathological myofibroblasts and adipocytes during muscular dystrophy and chronic muscle damage, but also important players for proper tissue regeneration. Their dysregulated activity during pathology impairs proper tissue repair. Our overall hypothesis is that efficient regeneration depends on a complex network of signaling interactions between multiple cell types leading to the proper coordination of their function. The best-known marker for FAPs is the receptor tyrosine kinase (RTK) plateletderived growth factor receptor alpha (PDGFRa). Several attempts to block the dysregulated RTK activity of PDGFRa in pathology have been successfully done, therefore, PDGFRa signaling emerges as a potential target against fibrosis. TGF-bmediated signaling pathways are commonly accepted to be fibrotic, to induce the proliferation of FAPs and myofibroblast differentiation from these precursors. TGF-b signaling and its ligands are augmented during DMD, and fibrosis in several tissues. Hence, TGF-b is a known driver of the fibrotic process. Here, we investigated the role of TGF-b signaling on PDGFRa expression and signaling, along with studying a functional cross-talk between PDGFRa and TGF-b in FAPs and MPCs. Canonical Wnt Tcf/Lef transcription factors are important players during development and controlling stem cell fate. Recently, the canonical Wnt signaling cascade emerged as a new system to study fibrosis in several tissues. Importantly, the role of Tcf/lef proteins in MPCs has not been studied yet. Additionally, whether TGF-b has an impact on Wnt signaling and/or may crosstalk through the regulation of these Wnt transcription factors has not been explored yet. In the present Ph.D. thesis, we focused on the TGF-b signaling pathway and its role in FAPs and MPCs. The main findings are; 1. MPCs are present in skeletal muscle under normal conditions and are increased in several models where muscle fibrosis and TGF-b are a hallmark. These Tcf7l2+ progenitors lie near macrophages mainly concentrated in dystrophic necrotic-regenerating foci. 2. We suggest that the historically named muscle CT fibroblasts isolated via pre-plating correspond to a phenotypically and biochemically FAPs-like population of adherent MPCs. These adherent cells respond in the same fashion to TGF-b signaling and the tyrosine kinase inhibitor Nilotinib as FAPs. 3. The role and/or cross-talk of TGF-b signaling in the regulation of PDGFRa expression and signaling in mesenchymal progenitors is described: i) PDGFRa expression is strongly reduced by TGF-b signaling in FAPs, Hic1+ MPs, skin fibroblasts, and two different MPs cell lines. ii) PDGFRa-mediated gene expression is altered during muscle regeneration in FAPs and after TGF-b1 treatment. iii) Pharmacological inhibition of PDGFRa impaired the TGF-b-mediated ECM remodeling and blocked the TGF-b1-induced migration of MPs. 4. the ubiquitin-proteasome system (UPS). Via Tcf7l2 pharmacological inhibition we suggest that Tcf7l2 plays a role in regulating FAPs survival and fate. Therefore, in this Ph.D. Thesis we studied and proposed that FAPs modulators and signaling governing pathways might be suitable for a novel therapeutic target for the treatment of MD, neurodegenerative diseases, non-malignant fibroproliferative disorders, and aging.Fibrosis, the dysregulated accumulation of connective tissue (CT), is a hallmark of multiple pathologies where inflammation is not fully resolved. The main components of the CT are the extracellular matrix (ECM) and its tissue-resident mesenchymal stromal cells (MSCs), which actively produce and remodel ECM during development, homeostasis, and disease. Fibrosis and/or fibro-fatty replacement of the functional tissue is a common feature of Duchenne Muscular Dystrophy (DMD), but it is also observed in neuromuscular diseases. It is generally accepted that these mesenchymal progenitor cells (MPCs) [hereafter referred to as fibro/adipogenic progenitors (FAPs)] are the progenitors of pathological myofibroblasts and adipocytes during muscular dystrophy and chronic muscle damage, but also important players for proper tissue regeneration. Their dysregulated activity during pathology impairs proper tissue repair. Our overall hypothesis is that efficient regeneration depends on a complex network of signaling interactions between multiple cell types leading to the proper coordination of their function. The best-known marker for FAPs is the receptor tyrosine kinase (RTK) plateletderived growth factor receptor alpha (PDGFRa). Several attempts to block the dysregulated RTK activity of PDGFRa in pathology have been successfully done, therefore, PDGFRa signaling emerges as a potential target against fibrosis. TGF-bmediated signaling pathways are commonly accepted to be fibrotic, to induce the proliferation of FAPs and myofibroblast differentiation from these precursors. TGF-b signaling and its ligands are augmented during DMD, and fibrosis in several tissues. Hence, TGF-b is a known driver of the fibrotic process. Here, we investigated the role of TGF-b signaling on PDGFRa expression and signaling, along with studying a functional cross-talk between PDGFRa and TGF-b in FAPs and MPCs. Canonical Wnt Tcf/Lef transcription factors are important players during development and controlling stem cell fate. Recently, the canonical Wnt signaling cascade emerged as a new system to study fibrosis in several tissues. Importantly, the role of Tcf/lef proteins in MPCs has not been studied yet. Additionally, whether TGF-b has an impact on Wnt signaling and/or may crosstalk through the regulation of these Wnt transcription factors has not been explored yet. In the present Ph.D. thesis, we focused on the TGF-b signaling pathway and its role in FAPs and MPCs. The main findings are; 1. MPCs are present in skeletal muscle under normal conditions and are increased in several models where muscle fibrosis and TGF-b are a hallmark. These Tcf7l2+ progenitors lie near macrophages mainly concentrated in dystrophic necrotic-regenerating foci. 2. We suggest that the historically named muscle CT fibroblasts isolated via pre-plating correspond to a phenotypically and biochemically FAPs-like population of adherent MPCs. These adherent cells respond in the same fashion to TGF-b signaling and the tyrosine kinase inhibitor Nilotinib as FAPs. 3. The role and/or cross-talk of TGF-b signaling in the regulation of PDGFRa expression and signaling in mesenchymal progenitors is described: i) PDGFRa expression is strongly reduced by TGF-b signaling in FAPs, Hic1+ MPs, skin fibroblasts, and two different MPs cell lines. ii) PDGFRa-mediated gene expression is altered during muscle regeneration in FAPs and after TGF-b1 treatment. iii) Pharmacological inhibition of PDGFRa impaired the TGF-b-mediated ECM remodeling and blocked the TGF-b1-induced migration of MPs. 4. the ubiquitin-proteasome system (UPS). Via Tcf7l2 pharmacological inhibition we suggest that Tcf7l2 plays a role in regulating FAPs survival and fate. Therefore, in this Ph.D. Thesis we studied and proposed that FAPs modulators and signaling governing pathways might be suitable for a novel therapeutic target for the treatment of MD, neurodegenerative diseases, non-malignant fibroproliferative disorders, and aging.Fibrosis, the dysregulated accumulation of connective tissue (CT), is a hallmark of multiple pathologies where inflammation is not fully resolved. The main components of the CT are the extracellular matrix (ECM) and its tissue-resident mesenchymal stromal cells (MSCs), which actively produce and remodel ECM during development, homeostasis, and disease. Fibrosis and/or fibro-fatty replacement of the functional tissue is a common feature of Duchenne Muscular Dystrophy (DMD), but it is also observed in neuromuscular diseases. It is generally accepted that these mesenchymal progenitor cells (MPCs) [hereafter referred to as fibro/adipogenic progenitors (FAPs)] are the progenitors of pathological myofibroblasts and adipocytes during muscular dystrophy and chronic muscle damage, but also important players for proper tissue regeneration. Their dysregulated activity during pathology impairs proper tissue repair. Our overall hypothesis is that efficient regeneration depends on a complex network of signaling interactions between multiple cell types leading to the proper coordination of their function. The best-known marker for FAPs is the receptor tyrosine kinase (RTK) plateletderived growth factor receptor alpha (PDGFRa). Several attempts to block the dysregulated RTK activity of PDGFRa in pathology have been successfully done, therefore, PDGFRa signaling emerges as a potential target against fibrosis. TGF-bmediated signaling pathways are commonly accepted to be fibrotic, to induce the proliferation of FAPs and myofibroblast differentiation from these precursors. TGF-b signaling and its ligands are augmented during DMD, and fibrosis in several tissues. Hence, TGF-b is a known driver of the fibrotic process. Here, we investigated the role of TGF-b signaling on PDGFRa expression and signaling, along with studying a functional cross-talk between PDGFRa and TGF-b in FAPs and MPCs. Canonical Wnt Tcf/Lef transcription factors are important players during development and controlling stem cell fate. Recently, the canonical Wnt signaling cascade emerged as a new system to study fibrosis in several tissues. Importantly, the role of Tcf/lef proteins in MPCs has not been studied yet. Additionally, whether TGF-b has an impact on Wnt signaling and/or may crosstalk through the regulation of these Wnt transcription factors has not been explored yet. In the present Ph.D. thesis, we focused on the TGF-b signaling pathway and its role in FAPs and MPCs. The main findings are; 1. MPCs are present in skeletal muscle under normal conditions and are increased in several models where muscle fibrosis and TGF-b are a hallmark. These Tcf7l2+ progenitors lie near macrophages mainly concentrated in dystrophic necrotic-regenerating foci. 2. We suggest that the historically named muscle CT fibroblasts isolated via pre-plating correspond to a phenotypically and biochemically FAPs-like population of adherent MPCs. These adherent cells respond in the same fashion to TGF-b signaling and the tyrosine kinase inhibitor Nilotinib as FAPs. 3. The role and/or cross-talk of TGF-b signaling in the regulation of PDGFRa expression and signaling in mesenchymal progenitors is described: i) PDGFRa expression is strongly reduced by TGF-b signaling in FAPs, Hic1+ MPs, skin fibroblasts, and two different MPs cell lines. ii) PDGFRa-mediated gene expression is altered during muscle regeneration in FAPs and after TGF-b1 treatment. iii) Pharmacological inhibition of PDGFRa impaired the TGF-b-mediated ECM remodeling and blocked the TGF-b1-induced migration of MPs. 4. the ubiquitin-proteasome system (UPS). Via Tcf7l2 pharmacological inhibition we suggest that Tcf7l2 plays a role in regulating FAPs survival and fate. Therefore, in this Ph.D. Thesis we studied and proposed that FAPs modulators and signaling governing pathways might be suitable for a novel therapeutic target for the treatment of MD, neurodegenerative diseases, non-malignant fibroproliferative disorders, and aging.Fibrosis, the dysregulated accumulation of connective tissue (CT), is a hallmark of multiple pathologies where inflammation is not fully resolved. The main components of the CT are the extracellular matrix (ECM) and its tissue-resident mesenchymal stromal cells (MSCs), which actively produce and remodel ECM during development, homeostasis, and disease. Fibrosis and/or fibro-fatty replacement of the functional tissue is a common feature of Duchenne Muscular Dystrophy (DMD), but it is also observed in neuromuscular diseases. It is generally accepted that these mesenchymal progenitor cells (MPCs) [hereafter referred to as fibro/adipogenic progenitors (FAPs)] are the progenitors of pathological myofibroblasts and adipocytes during muscular dystrophy and chronic muscle damage, but also important players for proper tissue regeneration. Their dysregulated activity during pathology impairs proper tissue repair. Our overall hypothesis is that efficient regeneration depends on a complex network of signaling interactions between multiple cell types leading to the proper coordination of their function. The best-known marker for FAPs is the receptor tyrosine kinase (RTK) plateletderived growth factor receptor alpha (PDGFRa). Several attempts to block the dysregulated RTK activity of PDGFRa in pathology have been successfully done, therefore, PDGFRa signaling emerges as a potential target against fibrosis. TGF-bmediated signaling pathways are commonly accepted to be fibrotic, to induce the proliferation of FAPs and myofibroblast differentiation from these precursors. TGF-b signaling and its ligands are augmented during DMD, and fibrosis in several tissues. Hence, TGF-b is a known driver of the fibrotic process. Here, we investigated the role of TGF-b signaling on PDGFRa expression and signaling, along with studying a functional cross-talk between PDGFRa and TGF-b in FAPs and MPCs. Canonical Wnt Tcf/Lef transcription factors are important players during development and controlling stem cell fate. Recently, the canonical Wnt signaling cascade emerged as a new system to study fibrosis in several tissues. Importantly, the role of Tcf/lef proteins in MPCs has not been studied yet. Additionally, whether TGF-b has an impact on Wnt signaling and/or may crosstalk through the regulation of these Wnt transcription factors has not been explored yet. In the present Ph.D. thesis, we focused on the TGF-b signaling pathway and its role in FAPs and MPCs. The main findings are; 1. MPCs are present in skeletal muscle under normal conditions and are increased in several models where muscle fibrosis and TGF-b are a hallmark. These Tcf7l2+ progenitors lie near macrophages mainly concentrated in dystrophic necrotic-regenerating foci. 2. We suggest that the historically named muscle CT fibroblasts isolated via pre-plating correspond to a phenotypically and biochemically FAPs-like population of adherent MPCs. These adherent cells respond in the same fashion to TGF-b signaling and the tyrosine kinase inhibitor Nilotinib as FAPs. 3. The role and/or cross-talk of TGF-b signaling in the regulation of PDGFRa expression and signaling in mesenchymal progenitors is described: i) PDGFRa expression is strongly reduced by TGF-b signaling in FAPs, Hic1+ MPs, skin fibroblasts, and two different MPs cell lines. ii) PDGFRa-mediated gene expression is altered during muscle regeneration in FAPs and after TGF-b1 treatment. iii) Pharmacological inhibition of PDGFRa impaired the TGF-b-mediated ECM remodeling and blocked the TGF-b1-induced migration of MPs. 4. the ubiquitin-proteasome system (UPS). Via Tcf7l2 pharmacological inhibition we suggest that Tcf7l2 plays a role in regulating FAPs survival and fate. Therefore, in this Ph.D. Thesis we studied and proposed that FAPs modulators and signaling governing pathways might be suitable for a novel therapeutic target for the treatment of MD, neurodegenerative diseases, non-malignant fibroproliferative disorders, and aging.
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    Role of Syndecan-4 in mouse development
    (2011) Escobedo Marambio, Noelia Andrea; Farias, Marjorie; Carrasco Saavedra, Héctor Patricio; Contreras Saavedra, Osvaldo Isaías; Tran, Uyen; Wessely, Oliver; Copp, Andrew; Larraín Correa, Juan Agustín
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    Single-cell revolution unveils the mysteries of the regenerative mammalian digit tip
    (2020) Riquelme Guzmán, Camilo; Contreras Saavedra, Osvaldo Isaías
    The digit tip is an exciting model for studying regeneration in mammals, but the precise mechanisms and the populations of cells involved in the formation and remodeling of the blastema remain unknown. In an exciting new work, Storer et al. take advantage of single-cell RNAseq combined with Pdgfra+ lineage-tracing to open the way into the enigmatic world of mammalian tissue regeneration.
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    Syndecan 4 interacts genetically with Vangl2 to regulate neural tube closure and planar cell polarity
    (2013) Escobedo, N.; Contreras Saavedra, Osvaldo Isaías; Valle Muñoz Videla, Rosana del; Farías, M.; Carrasco Saavedra, Héctor Patricio; Hill, C.; Tran, U.; Pryor, S.; Wessely, O.; Copp, A.; Larraín Correa, Juan Agustín
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    TGF-β-driven downregulation of the transcription factor TCF7L2 affects Wnt/β-catenin signaling in PDGFRα+ fibroblasts
    (2020) Contreras Saavedra, Osvaldo Isaías; Soliman, Hesham; Theret, Marine; Rossi, Fabio M. V.; Brandan, Enrique
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    Transforming growth factor type-b inhibits Masreceptor expression in fibroblasts but not inmyoblasts or differentiated myotubes; Relevanceto fibrosis associated to muscular dystrophies
    (2015) Cofré, Catalina; Acuña, María José; Contreras, Osvaldo; Morales, María Gabriela; Riquelme Illanes, Cecilia Angélica; Cabello Verrugio, Claudio Alejandro; Brandan, Enrique; Cofré, Catalina; Acuña, María José; Contreras Saavedra, Osvaldo Isaías; Morales, María Gabriela; Riquelme Illanes, Cecilia Angélica; Cabello Verrugio, Claudio Alejandro; Brandan, Enrique