Human and animal cells under influence of different lighting and stimulus

Eric Almeida, Eric Almeida Xavier, Anelise Freitas, Isabela Canavezzi Matias
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Abstract

Circadian rhythms, are the basis of homeostasis of organisms like human and other mammals. Violation of circadian rhythms leads to the development of pathological conditions and severe course of preexisting pathologies. For example some work with B16-F1O cells (B16) has shown that molecules like opsins, Circadian Locomotor Output Cycles Kaput (CLOCK) and clock genes are changed after a white light pulse (WLP). Like this, melanopsin (OPN4) and rhodopsin (OPN2) through UVA irradiation induced B16 pigmentation. Thus, heat shock reduces secreted rhodopsin expression in normal Melan-a melanocytes, while the opposite effect is found in malignant B16 cells. In both cell lines UVA radiation increases the expression of melanopsin and melanin, interfering with several clock genes, and also increasing the DNA repair enzyme xeroderma pigmentosum, complementation group A (XPA). Furthermore, B16 are more responsive to UVA radiation when compared to normal cells. Thereby, opsins are involved in animal camouflage. And their functions in humans involve different wavelengths, for example in skin the keratinocyte differentiation by (410 nm) involved cone opsin (OPN1) and rhodopsin (OPN2), like this in epidermal keratinocytes irradiation by (447 nm) accelerates closure in wound-healing and violet light (415 nm) induced hyperpigmentation. Furthermore, in B16 cell culture certain wavelengths induce proliferation or inhibition like signs of apoptosis and necrosis. Finally understanding the response of opsins and clock genes to different wavelengths in the skin, we could attribute a therapeutic of photobiomodulation (PBM) to approach various dermatological conditions, such as psoriasis, atopic dermatitis, hair growth, wound healing and tissue regeneration.
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不同光照和刺激影响下的人类和动物细胞
昼夜节律是人类和其他哺乳动物等生物体平衡的基础。违反昼夜节律会导致病理状态的发展和原有病理状态的严重恶化。例如,对 B16-F1O 细胞(B16)进行的一些研究表明,在白光脉冲(WLP)作用下,光蛋白、昼夜节律运动输出周期(CLOCK)和时钟基因等分子会发生变化。与此类似,黑视蛋白(OPN4)和红视蛋白(OPN2)通过 UVA 照射诱导 B16 色素沉着。因此,在正常的 Melan-a 黑色素细胞中,热休克会降低分泌的视紫红质的表达,而在恶性 B16 细胞中则出现相反的效果。在这两种细胞系中,UVA 辐射都会增加黑色素视蛋白和黑色素的表达,干扰多个时钟基因,并增加 DNA 修复酶色素沉着病互补组 A(XPA)的表达。此外,与正常细胞相比,B16 对 UVA 辐射的反应更为敏感。因此,蛋白参与了动物的伪装。例如,在皮肤角质细胞分化过程中,波长为 410 纳米的锥形视蛋白(OPN1)和视紫红质(OPN2)参与了角质细胞分化,同样,在表皮角质细胞中,波长为 447 纳米的辐照可加速伤口愈合,而波长为 415 纳米的紫光可诱导色素沉着。此外,在 B16 细胞培养中,某些波长的光线会诱导细胞增殖或抑制细胞凋亡和坏死。通过了解皮肤中的蛋白和时钟基因对不同波长的反应,我们可以将光生物调节(PBM)疗法用于治疗各种皮肤病,如牛皮癣、特应性皮炎、毛发生长、伤口愈合和组织再生。
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