Discovery of a novel ingredient that regulates the expression of senescent fibroblasts-related aging marker and the dendritic changes of melanocytes caused by nerve fiber
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Presented by: Soyoun Lee
Dark spot or aged spot are hyperpigmented macules of skin that usually formed after long-term exposure to ultraviolet radiation, but they can be caused by other things, too. Skin conditions, pregnancy and certain medications or medical conditions may cause dark spots. To reduce dark spots, most cosmetic ingredients have used a strategy to reduce melanin production so far. In a recent study, it was revealed that dark spots are caused by the accumulation of a large number of senescent fibroblasts at the sites of pigmentation. The suppression of stromal-derived factor 1 (SDF-1) expression in senescence fibroblasts promotes melanocyte melanin production. Also, another study reported that the density of the nerve fiber affects the process of continuous regeneration even when the dark spot is removed.
In our previous study results, we discovered four aging markers that act on the 1st aging peak. Among these aging markers, it was confirmed that the expression of GDF15 was increased in aged skin fibroblasts. We tried to confirm that the aging marker GDF15 discovered by us can also affect dark spots, based on the previous study on the effect of aging fibrolasts on dark spots. Based on these studies, we develop the ingredients using a new strategy to prevent the generation and recurrence of dark spots by acting on senescence fibroblasts and nerve fibers.
To investigate the regulatory role played by senescent fibroblasts on melanocytes, SDF-1 and GDF15 mRNA expression levels were detected by qRT-PCR. In addition, to confirm whether the dendritic extension of melanocytes is suppressed, a culture medium of nerve cells with or without a new ingredient was added to melanocytes. To improve dark spots, it is ultimately necessary to decrease melanin contents in the pigmented area, so we evaluated whether our new ingredient could inhibit melanin synthesis.
As a result, the expression of SDF-1 mRNA was inhibited in UVA-induced senescent fibroblasts. In addition, it was confirmed that the increased GDF15 in senescent fibroblasts activates melanogenesis in melanocytes. While a new ingredient can increase the expression of SDF-1 and inhibited the expression of GDF15 in senescent fibroblast. Also, the dendritic of melanocytes had been reduced by a culture medium of nerve cells with a new ingredient was added to melanocytes. Furthermore, the material decreased the expression of MITF, TRP1, and inhibited melanin contents in melanocytes.
We found that GDF15, one of the aging markers we expressed, is related to the aging phenomenon in which dark spots on the skin increase with agin. Our new ingredient has a dark spot-specific care activity by reducing the effects of senescent fibroblasts and nerve fibers on melanocytes. Through this effect, as a result, our new material can reduce the melanin content in the dark spot area as well as inhibit the dark spot regeneration by nerve cells.
In our previous study results, we discovered four aging markers that act on the 1st aging peak. Among these aging markers, it was confirmed that the expression of GDF15 was increased in aged skin fibroblasts. We tried to confirm that the aging marker GDF15 discovered by us can also affect dark spots, based on the previous study on the effect of aging fibrolasts on dark spots. Based on these studies, we develop the ingredients using a new strategy to prevent the generation and recurrence of dark spots by acting on senescence fibroblasts and nerve fibers.
To investigate the regulatory role played by senescent fibroblasts on melanocytes, SDF-1 and GDF15 mRNA expression levels were detected by qRT-PCR. In addition, to confirm whether the dendritic extension of melanocytes is suppressed, a culture medium of nerve cells with or without a new ingredient was added to melanocytes. To improve dark spots, it is ultimately necessary to decrease melanin contents in the pigmented area, so we evaluated whether our new ingredient could inhibit melanin synthesis.
As a result, the expression of SDF-1 mRNA was inhibited in UVA-induced senescent fibroblasts. In addition, it was confirmed that the increased GDF15 in senescent fibroblasts activates melanogenesis in melanocytes. While a new ingredient can increase the expression of SDF-1 and inhibited the expression of GDF15 in senescent fibroblast. Also, the dendritic of melanocytes had been reduced by a culture medium of nerve cells with a new ingredient was added to melanocytes. Furthermore, the material decreased the expression of MITF, TRP1, and inhibited melanin contents in melanocytes.
We found that GDF15, one of the aging markers we expressed, is related to the aging phenomenon in which dark spots on the skin increase with agin. Our new ingredient has a dark spot-specific care activity by reducing the effects of senescent fibroblasts and nerve fibers on melanocytes. Through this effect, as a result, our new material can reduce the melanin content in the dark spot area as well as inhibit the dark spot regeneration by nerve cells.