3D Bioprinted Aging Skin Model

3D Bioprinted Aging Skin Model

A wide constellation of factors like cellular senescence marked with the transformation of active ECM synthesizing fibroblast cells to senescent phenotype and loss of elastic property of collagen in the ECM of the skin causes a reduction in skin tissue functionality, a significant hallmark in the skin aging process. The three-dimensional tissue model of human skin aging developed by us exhibits anatomical relevance to aged skin and expresses aged-skin-related biomarkers depicting the desirable physiological function.


Expression of ECM protein fibronectin, a hallmark of aged skin phenotype


  1. Cell-cycle arrest: BrdU labeling of cells indicated a decreasing order signifying stagnating cell growth, which was further corroborated by an increasing trend of p21 mRNA levels, an indicator of cell-cycle arrest.
  1. Cellular senescence: Senescence-associated beta-galactosidase marker was used to validate induction of senescence in fibroblast cells which showed an increasing trend.
  1. Epidermal thickness: Histological analysis by H&E staining demonstrated a reduced epithermal thickness, a characteristic feature of aged skin.
  1. Protein expression: Immunohistochemical analysis of early & late fibroblast differentiation markers (Keratin10 and Filaggrin) showed a decreased protein expression indicating the role of senescent fibroblast in the dysregulated differentiation process
  1. Barrier integrity: Biotin permeability assay performed to evaluate the permeability of aging skin tissue depicted defective barrier integrity in the fabricated tissue model. Contact angle measurement also demonstrated similar outcomes elucidating the role of senescent fibroblast in enhanced permeability of aged skin.

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