Abstract
Skin aging is the result of superimposed intrinsic (individual) and extrinsic (e.g., UV exposure or nutrition) aging. Previous works have reported a relationship between UV irradiation and glycation in the aging process, leading, for example, to modified radical species production and the appearance of AGEs (advanced glycosylation end products) in increasing quantities, particularly glycoxidation products like pentosidine. In addition, the colocalization of AGEs and elastosis has also been observed. We first investigated the combination of the glycation reaction and UVA effects on a reconstructed skin model to explain their cumulative biological effect. We found that UVA exposure combined with glycation had the ability to intensify the response for specific markers: for example, MMP1 or MMP3 mRNA, proteases involved in extracellular matrix degradation, or proinflammatory cytokine, IL1α, protein expression. Moreover, the association of glycation and UVA irradiation is believed to promote an environment that favors the onset of an elastotic-like phenomenon: mRNA coding for elastin, elastase, and tropoelastin expression is increased. Secondly, because the damaging effects of UV radiation in vivo might be more detrimental in aged skin than in young skin due to increased accumulation of pentosidine and the exacerbation of alterations related to chronological aging, we studied the biological effect of soluble pentosidine in fibroblasts grown in monolayers. We found that pentosidine induced upregulation of CXCL2, IL8, and MMP12 mRNA expression (inflammatory and elastotic markers, respectively). Tropoelastin protein expression (elastin precursor) was also increased. In conclusion, fibroblasts in monolayers cultured with soluble pentosidine and tridimensional in vitro skin constructs exposed to the combination of AGEs and UVA promote an inflammatory state and an alteration of the dermal compartment in relation to an elastosis-like environment.
Highlights
Chronological or intrinsic aging constitutes the individual and genetic mechanism of aging
To estimate the presence of the glycation products in the collagen solution, fluorescence is measured at the end of incubation with the sugar. e fluorescence measurment in the sample containing collagen modified by glycation was higher (×12 and × 4 at λex 335 nm/λem 385 nm and λex 370 nm/λem 440 nm, respectively) than in the control sample incubated without ribose (Figures 1(a) and 1(b)). is procedure allows to reveal the presence of AGEs in the collagen modified by glycation
In the culture medium of reconstructed skin after 48 hours post-UVA exposure, a 1.5-fold increase in IL1α secretion was observed in the culture medium of native in vitro skin induced by irradiation (N0 vs. N10) and strongly amplified by glycation products (G0 vs. G10) (3-fold, p 0.0003) (Figure 2(f )). is effect was observed with the 4 batches of fibroblasts used (Figure 2(e))
Summary
Chronological or intrinsic aging constitutes the individual and genetic mechanism of aging. A well-known reaction which appears during chronological aging is the glycation reaction. E presence of these products in the skin changes the physical, biomechanical (stiffening and loss of elasticity), and biological properties (modulation of synthesis and degradation of the matrix by cells) [2]. Another cause of the skin aging process is extrinsic aging, caused by different external factors like UVR (UV radiation and photoaging). Is process contributes to the aging mechanism and leads to the elastosis zone in the dermis and to the formation of wrinkles. After UV irradiation, the stimulation of collagen breakdown and inhibition of procollagen synthesis causing loss of collagen
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