Abstract

The dermis is largely composed of collagen-rich fibrils that form a dense extracellular matrix (ECM). Dermal fibroblasts produce and are embedded within the dermal ECM. During aging, the ECM becomes fragmented. This fragmentation is associated with deleterious alterations of fibroblast function. We have investigated the degree to which these alterations stem from adaptation to dermal ECM deterioration versus cell-autonomous age-driven responses. Primary dermal fibroblasts from young (20-30 years old, 6 females, 6 males) and aged (>80 years old, 6 females, 6 males) individuals were placed in standard monolayer culture and either harvested at 70% confluence (P1) for telomere quantitation and RNAseq transcriptome analysis or cultured through multiple passages.

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