Abstract
Understanding the contribution of the dermis in skin aging is a key question, since this tissue is particularly important for skin integrity, and because its properties can affect the epidermis. Characteristics of matched pairs of dermal papillary and reticular fibroblasts (Fp and Fr) were investigated throughout aging, comparing morphology, secretion of cytokines, MMPs/TIMPs, growth potential, and interaction with epidermal keratinocytes. We observed that Fp populations were characterized by a higher proportion of small cells with low granularity and a higher growth potential than Fr populations. However, these differences became less marked with increasing age of donors. Aging was also associated with changes in the secretion activity of both Fp and Fr. Using a reconstructed skin model, we evidenced that Fp and Fr cells do not possess equivalent capacities to sustain keratinopoiesis. Comparing Fp and Fr from young donors, we noticed that dermal equivalents containing Fp were more potent to promote epidermal morphogenesis than those containing Fr. These data emphasize the complexity of dermal fibroblast biology and document the specific functional properties of Fp and Fr. Our results suggest a new model of skin aging in which marked alterations of Fp may affect the histological characteristics of skin.
Highlights
Chronological aging is described as a time-dependant biological process leading to gradual changes in the structure and functions of all tissues that compose an organism
Because fibroblasts which reside in the dermis can both produce and degrade extracellular matrix components, exploration of the possible evolution of their properties throughout aging is important to progress in the understanding of this complex process
This study was conducted to explore the possibility that fibroblast sub-populations which reside within the superficial and the deep regions of the dermis, respectively papillary and reticular fibroblasts (Fp and Fr), may play different roles in skin aging
Summary
Chronological aging is described as a time-dependant biological process leading to gradual changes in the structure and functions of all tissues that compose an organism. These modifications tend to decrease the capacity for adaptive responsiveness and wound healing, and enhance its susceptibility to disorders and death. Genetic diseases which display clinical signs of premature aging such as progeroid syndromes are an important source of information to identify molecular effectors involved in aging [2]. The importance of specific allelic polymorphisms in the predisposition of human beings to longevity or resistance to agerelated disorders has been emphasized by studies of centenarians [3]. In addition to intrinsic genetic factors, chronological aging is controlled through epigenetic mechanisms and is affected by environmental parameters including nutrition [4], which clearly leads to consider this biological process as a complex multifactorial phenomenon
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