Your browser doesn't support javascript.
loading
Fibroblast senescence-associated extracellular matrix promotes heterogeneous lung niche.
Howes, Andrew M; Dea, Nova C; Ghosh, Deepraj; Krishna, Krishangi; Wang, Yihong; Li, Yanxi; Morrison, Braxton; Toussaint, Kimani C; Dawson, Michelle R.
Afiliación
  • Dea NC; Department of Molecular Biology, Cell Biology, and Biochemistry, Brown University, Providence, Rhode Island 029012, USA.
  • Ghosh D; Department of Molecular Biology, Cell Biology, and Biochemistry, Brown University, Providence, Rhode Island 029012, USA.
  • Krishna K; School of Engineering, Brown University, Providence, Rhode Island 02912, USA.
  • Wang Y; Department of Pathology and Laboratory Medicine, Brown University, Providence, Rhode Island 02912, USA.
  • Li Y; Department of Molecular Biology, Cell Biology, and Biochemistry, Brown University, Providence, Rhode Island 029012, USA.
  • Morrison B; Department of Molecular Biology, Cell Biology, and Biochemistry, Brown University, Providence, Rhode Island 029012, USA.
  • Toussaint KC; School of Engineering, Brown University, Providence, Rhode Island 02912, USA.
  • Dawson MR; Department of Molecular Biology, Cell Biology, and Biochemistry, Brown University, Providence, Rhode Island 029012, USA.
APL Bioeng ; 8(2): 026119, 2024 Jun.
Article en En | MEDLINE | ID: mdl-38855444
ABSTRACT
Senescent cell accumulation in the pulmonary niche is associated with heightened susceptibility to age-related disease, tissue alterations, and ultimately a decline in lung function. Our current knowledge of senescent cell-extracellular matrix (ECM) dynamics is limited, and our understanding of how senescent cells influence spatial ECM architecture changes over time is incomplete. Herein is the design of an in vitro model of senescence-associated extracellular matrix (SA-ECM) remodeling using a senescent lung fibroblast-derived matrix that captures the spatiotemporal dynamics of an evolving senescent ECM architecture. Multiphoton second-harmonic generation microscopy was utilized to examine the spatial and temporal dynamics of fibroblast SA-ECM remodeling, which revealed a biphasic process that established a disordered and heterogeneous architecture. Additionally, we observed that inhibition of transforming growth factor-ß signaling during SA-ECM remodeling led to improved local collagen fiber organization. Finally, we examined patient samples diagnosed with pulmonary fibrosis to further tie our results of the in vitro model to clinical outcomes. Moreover, we observed that the senescence marker p16 is correlated with local collagen fiber disorder. By elucidating the temporal dynamics of SA-ECM remodeling, we provide further insight on the role of senescent cells and their contributions to pathological ECM remodeling.

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Idioma: En Revista: APL Bioeng Año: 2024 Tipo del documento: Article Pais de publicación: Estados Unidos

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Idioma: En Revista: APL Bioeng Año: 2024 Tipo del documento: Article Pais de publicación: Estados Unidos