Summary Our skin is regularly exposed to UV radiation from the sun. Chronic, meaning long‐term, exposure to UV radiation (mainly a type of UV called UVA) causes an increase in enzymes called matrix metalloproteinases (MMPs), especially MMP1, MMP2, MMP3 and MMP9, in skin cells called human dermal fibroblasts (HDFs). MMPs can lead to the breakdown of fibrous connective tissue which gives the skin its support and structure, and this is the most important cause of skin photo‐aging (skin aging caused by UV). We don't exactly know how, on a molecular level, fibroblasts sense UVA and trigger signals via cells to MMPs. This study looked at a type of protein in the body called Opsins (OPNs) which can change their signaling pathways (how they communicate with other cells) in response to being hit by light. OPNs play a vital role in our sight, circadian rhythm (our sleep‐wake cycle) and how the eye's pupil responds to light. This study provides evidence that a type of OPNs called OPN3 plays a role in the production of MMP1, MMP2, MMP3 and MMP9 in HDFs following UVA exposure. This provide insights into the understanding of the molecular mechanisms through which human skin cells respond to UVA radiation, and may reveal molecular targets for preventing or treating skin photo‐ageing. This is a summary of the study: Opsin 3 is a key regulator of ultraviolet A‐induced photoageing in human dermal fibroblast cells.
Summary 我们的皮肤经常暴露于阳光中的紫外线 辐射下。长期暴露于紫外线辐射(主要是一种称为 UVA 的紫外线)会使称为人真皮成纤维细胞 (HDF) 的皮肤细胞中的基质金属蛋白酶 (MMP) 增加,尤其是 MMP1、MMP2、MMP3 和 MMP9。 MMP 可导致为皮肤提供支撑和结构的纤维结缔组织分解,而这是皮肤光老化(由紫外线引起的皮肤老化)的最重要原因。 我们并不清楚在分子水平上,成纤维细胞如何感觉 UVA,并通过细胞触发信号传导至 MMP。 本研究分析了体内一种称为 Opsin (OPN) 的蛋白质,这种蛋白质可以改变其信号通路(它们如何与其他细胞交流),对光线照射做出反应。OPN 在我们的视力、昼夜节律(我们的睡眠‐觉醒周期)以及眼睛瞳孔对光的反应中起着重要作用。 这项研究证明,一种称为 OPN3 的 OPN 在 UVA 暴露后,在 HDF 中的 MMP1、MMP2、MMP3 和 MMP9 产生中发挥作用。这提供了对人类皮肤细胞对 UVA 辐射反应的分子机制的了解,并可能揭示预防或治疗皮肤光老化的分子靶标。 本摘要涉及研究:Opsin 3 是人真皮成纤维细胞中紫外线 A 诱导光老化的关键调节因子。
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