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  1. AU="Fraczek, Paula M"
  2. AU="Fritz, Cassandra Dl"
  3. AU="Sommer, Norbert"
  4. AU="Brandão, Claudia Valeria S"
  5. AU="Jesky, Mark D"
  6. AU="Filipe de Oliveira"
  7. AU="Chang, Shantel"
  8. AU="Mbow, M Lamine"
  9. AU="Sekhon, M."
  10. AU="Song, Y-S"
  11. AU="Collins, Brooke"
  12. AU="Ali Al-Naji"
  13. AU="Bansal, Bhavtosh"
  14. AU="De Cremer, Kaat"
  15. AU="O'Neil, James"
  16. AU=White Tonya
  17. AU="Clark-Deener, Sherrie"
  18. AU="Ishak Yassir"
  19. AU="Chih-Wei Chen"

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  1. Artikel ; Online: Three-dimensional chromatin re-organization during muscle stem cell aging.

    Yang, Benjamin A / Larouche, Jacqueline A / Sabin, Kaitlyn M / Fraczek, Paula M / Parker, Stephen C J / Aguilar, Carlos A

    Aging cell

    2023  Band 22, Heft 4, Seite(n) e13789

    Abstract: Age-related skeletal muscle atrophy or sarcopenia is a significant societal problem that is becoming amplified as the world's population continues to increase. The regeneration of damaged skeletal muscle is mediated by muscle stem cells, but in old age ... ...

    Abstract Age-related skeletal muscle atrophy or sarcopenia is a significant societal problem that is becoming amplified as the world's population continues to increase. The regeneration of damaged skeletal muscle is mediated by muscle stem cells, but in old age muscle stem cells become functionally attenuated. The molecular mechanisms that govern muscle stem cell aging encompass changes across multiple regulatory layers and are integrated by the three-dimensional organization of the genome. To quantitatively understand how hierarchical chromatin architecture changes during muscle stem cell aging, we generated 3D chromatin conformation maps (Hi-C) and integrated these datasets with multi-omic (chromatin accessibility and transcriptome) profiles from bulk populations and single cells. We observed that muscle stem cells display static behavior at global scales of chromatin organization during aging and extensive rewiring of local contacts at finer scales that were associated with variations in transcription factor binding and aberrant gene expression. These data provide insights into genome topology as a regulator of molecular function in stem cell aging.
    Mesh-Begriff(e) Genome ; Cellular Senescence/genetics ; Chromatin/genetics ; Muscle, Skeletal
    Chemische Substanzen Chromatin
    Sprache Englisch
    Erscheinungsdatum 2023-02-02
    Erscheinungsland England
    Dokumenttyp Journal Article ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2113083-8
    ISSN 1474-9726 ; 1474-9718
    ISSN (online) 1474-9726
    ISSN 1474-9718
    DOI 10.1111/acel.13789
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  2. Artikel: Manipulation of the nucleoscaffold potentiates cellular reprogramming kinetics.

    Yang, Benjamin A / da Rocha, André Monteiro / Newton, Isabel / Shcherbina, Anna / Wong, Sing-Wan / Fraczek, Paula M / Larouche, Jacqueline A / Hiraki, Harrison L / Baker, Brendon M / Shin, Jae-Won / Takayama, Shuichi / Thouless, M D / Aguilar, Carlos A

    bioRxiv : the preprint server for biology

    2023  

    Abstract: Somatic cell fate is an outcome set by the activities of specific transcription factors and the chromatin landscape and is maintained by gene silencing of alternate cell fates through physical interactions with the nuclear scaffold. Here, we evaluate the ...

    Abstract Somatic cell fate is an outcome set by the activities of specific transcription factors and the chromatin landscape and is maintained by gene silencing of alternate cell fates through physical interactions with the nuclear scaffold. Here, we evaluate the role of the nuclear scaffold as a guardian of cell fate in human fibroblasts by comparing the effects of transient loss (knockdown) and mutation (progeria) of functional Lamin A/C, a core component of the nuclear scaffold. We observed that Lamin A/C deficiency or mutation disrupts nuclear morphology, heterochromatin levels, and increases access to DNA in lamina-associated domains. Changes in Lamin A/C were also found to impact the mechanical properties of the nucleus when measured by a microfluidic cellular squeezing device. We also show that transient loss of Lamin A/C accelerates the kinetics of cellular reprogramming to pluripotency through opening of previously silenced heterochromatin domains while genetic mutation of Lamin A/C into progerin induces a senescent phenotype that inhibits the induction of reprogramming genes. Our results highlight the physical role of the nuclear scaffold in safeguarding cellular fate.
    Sprache Englisch
    Erscheinungsdatum 2023-03-13
    Erscheinungsland United States
    Dokumenttyp Preprint
    DOI 10.1101/2023.03.12.532246
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  3. Artikel ; Online: Maresin 1 repletion improves muscle regeneration after volumetric muscle loss.

    Castor-Macias, Jesus A / Larouche, Jacqueline A / Wallace, Emily C / Spence, Bonnie D / Eames, Alec / Duran, Pamela / Yang, Benjamin A / Fraczek, Paula M / Davis, Carol A / Brooks, Susan V / Maddipati, Krishna Rao / Markworth, James F / Aguilar, Carlos A

    eLife

    2023  Band 12

    Abstract: The acute traumatic or surgical loss of skeletal muscle, known as volumetric muscle loss (VML), is a devastating type of injury that results in exacerbated and persistent inflammation followed by fibrosis. The mechanisms that mediate the magnitude and ... ...

    Abstract The acute traumatic or surgical loss of skeletal muscle, known as volumetric muscle loss (VML), is a devastating type of injury that results in exacerbated and persistent inflammation followed by fibrosis. The mechanisms that mediate the magnitude and duration of the inflammatory response and ensuing fibrosis after VML remain understudied, and as such, the development of regenerative therapies has been limited. To address this need, we profiled how lipid mediators, which are potent regulators of the immune response after injury, varied with VML injuries that heal or result in fibrosis. We observed that non-healing VML injuries displayed increased pro-inflammatory eicosanoids and a lack of pro-resolving lipid mediators. Treatment of VML with a pro-resolving lipid mediator synthesized from docosahexaenoic acid, called Maresin 1, ameliorated fibrosis through reduction of neutrophils and macrophages and enhanced recovery of muscle strength. These results expand our knowledge of the dysregulated immune response that develops after VML and identify a novel immuno-regenerative therapeutic modality in Maresin 1.
    Mesh-Begriff(e) Humans ; Docosahexaenoic Acids ; Muscle, Skeletal/physiology ; Muscular Diseases/pathology ; Fibrosis
    Chemische Substanzen 7,14-dihydroxydocosa-4,8,10,12,16,19-hexaenoic acid ; Docosahexaenoic Acids (25167-62-8)
    Sprache Englisch
    Erscheinungsdatum 2023-12-22
    Erscheinungsland England
    Dokumenttyp Journal Article
    ZDB-ID 2687154-3
    ISSN 2050-084X ; 2050-084X
    ISSN (online) 2050-084X
    ISSN 2050-084X
    DOI 10.7554/eLife.86437
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  4. Artikel ; Online: Neutrophil and natural killer cell imbalances prevent muscle stem cell-mediated regeneration following murine volumetric muscle loss.

    Larouche, Jacqueline A / Fraczek, Paula M / Kurpiers, Sarah J / Yang, Benjamin A / Davis, Carol / Castor-Macias, Jesus A / Sabin, Kaitlyn / Anderson, Shannon / Harrer, Julia / Hall, Matthew / Brooks, Susan V / Jang, Young C / Willett, Nick / Shea, Lonnie D / Aguilar, Carlos A

    Proceedings of the National Academy of Sciences of the United States of America

    2022  Band 119, Heft 15, Seite(n) e2111445119

    Abstract: Volumetric muscle loss (VML) overwhelms the innate regenerative capacity of mammalian skeletal muscle (SkM), leading to numerous disabilities and reduced quality of life. Immune cells are critical responders to muscle injury and guide tissue resident ... ...

    Abstract Volumetric muscle loss (VML) overwhelms the innate regenerative capacity of mammalian skeletal muscle (SkM), leading to numerous disabilities and reduced quality of life. Immune cells are critical responders to muscle injury and guide tissue resident stem cell– and progenitor-mediated myogenic repair. However, how immune cell infiltration and intercellular communication networks with muscle stem cells are altered following VML and drive pathological outcomes remains underexplored. Herein, we contrast the cellular and molecular mechanisms of VML injuries that result in the fibrotic degeneration or regeneration of SkM. Following degenerative VML injuries, we observed the heightened infiltration of natural killer (NK) cells as well as the persistence of neutrophils beyond 2 wk postinjury. Functional validation of NK cells revealed an antagonistic role in neutrophil accumulation in part via inducing apoptosis and CCR1-mediated chemotaxis. The persistent infiltration of neutrophils in degenerative VML injuries was found to contribute to impairments in muscle stem cell regenerative function, which was also attenuated by transforming growth factor beta 1 (TGFβ1). Blocking TGFβ signaling reduced neutrophil accumulation and fibrosis and improved muscle-specific force. Collectively, these results enhance our understanding of immune cell–stem cell cross talk that drives regenerative dysfunction and provide further insight into possible avenues for fibrotic therapy exploration.
    Mesh-Begriff(e) Animals ; Fibrosis ; Killer Cells, Natural/immunology ; Mice ; Muscle, Skeletal/immunology ; Muscle, Skeletal/pathology ; Muscular Diseases/immunology ; Muscular Diseases/pathology ; Neutrophil Infiltration ; Neutrophils/immunology ; Regeneration/immunology ; Satellite Cells, Skeletal Muscle/immunology ; Transforming Growth Factor beta/metabolism
    Chemische Substanzen Transforming Growth Factor beta
    Sprache Englisch
    Erscheinungsdatum 2022-04-04
    Erscheinungsland United States
    Dokumenttyp Journal Article
    ZDB-ID 209104-5
    ISSN 1091-6490 ; 0027-8424
    ISSN (online) 1091-6490
    ISSN 0027-8424
    DOI 10.1073/pnas.2111445119
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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    Verfügbar in ZB MED Köln/Königswinter

    Zs.A 1148: Hefte anzeigen Standort:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

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    Dieser Service ist kostenpflichtig (siehe Lieferbedingungen von subito). Bestellungen, die einen Artikel nebst Supplementary Material umfassen, werden grundsätzlich wie mehrfache Bestellungen bearbeitet. Gebühren fallen in diesen Fällen für jede einzelne Bestellung an.

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