UV-induced senescence of human dermal fibroblasts restrained by low-stiffness matrix by inhibiting NF-κB activation

• PDMS substrates with tunable stiffness coated by fibronectin are rational designed and fabricated. HDFs were more sensitive to UV induced ROS accumulation cell senescence on stiff substrates. Soft significantly reduced production senescence. ECM plays a significant regulatory role As hallmark of skin ageing, senescent human dermal fibroblasts (HDFs) known lose the ability divide. However, they can still interact their cellular environment surrounding matrix. ages, progressive slowing down function decreases skin's structural integrity, which is serious than if there collagen matrix eroded. This leads matte r s unbalanced barrier under skin, fragility, inadequate wound healing, as well other cosmetic issues. It also documented that ageing comes increases. Therefore, understanding interactions between microenvironments during may provide insights into ageing. Here we aim investigate stiffness' effect HDF elucidate possible mechanisms make senescent. In our experiments, cultivated Polydimethylsiloxane (PDMS) various stiffnesses exposed light trigger Results show affected when cultured stiffness. cells not low The following characterization revealed exposure had stimulated nucleus factor kappa-B (NF-κB) activation. contrast, softness only displayed activation NF-κB. NF-κB activity suppression ammonium pyrrolidine dithiocarbamate (PDTC) UV-induced Taken together, demonstrated soft defends against ultraviolet-induced inhibiting