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Sox9 Accelerates Vascular Aging by Regulating Extracellular Matrix Composition and Stiffness.

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Cellular senescence and stiffening extracellular matrix (ECM) promote Sox9 expression, which drives further ECM modifications, accelerating vascular aging. This study reveals a feedback cycle in vascular aging.

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Area of Science:

  • Vascular Biology
  • Cellular Aging
  • Biomaterials Science

Background:

  • Vascular calcification and increased extracellular matrix (ECM) stiffness are key features of vascular aging.
  • Sox9 (SRY-box transcription factor 9) is linked to vascular smooth muscle cell (VSMC) osteo/chondrogenic conversion, but its role in aging and calcification is unknown.

Purpose of the Study:

  • To investigate the relationship between Sox9, vascular aging, and ECM properties.
  • To elucidate the role of Sox9 in regulating VSMC phenotype and ECM characteristics during aging.

Main Methods:

  • Immunohistochemistry on human aortic samples from young and aged patients.
  • In vitro studies using young and senescent VSMCs, manipulating Sox9 expression.
  • Characterization of ECM properties using atomic force microscopy and proteomics.
  • Assessment of VSMC phenotype on engineered matrices.

Main Results:

  • Sox9 correlated with the senescence marker p16 in vivo and showed mechanosensitive expression in senescent cells and stiff matrices in vitro.
  • Sox9 regulated ECM stiffness and organization by altering collagen expression and reducing VSMC contractility.
  • Sox9 targeted LH3 (procollagen-lysine, 2-oxoglutarate 5-dioxygenase 3), a key regulator of ECM stiffness, and promoted its deposition via extracellular vesicles.

Conclusions:

  • Sox9 plays a crucial role in regulating ECM structure and composition, influencing VSMC phenotype.
  • A positive feedback loop exists where senescence and ECM stiffening promote Sox9, which further enhances stiffening and senescence.
  • Findings highlight the importance of ECM in regulating VSMC phenotype and suggest therapeutic targets for vascular aging.