人皮肤成纤维细胞对l -抗坏血酸的年龄相关反应:I型和III型胶原合成的研究。

M Dumas, C Chaudagne, F Bonté, A Meybeck
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引用次数: 0

摘要

研究了0.15 mM l -抗坏血酸(AA)对30例19 ~ 70岁女性真皮成纤维细胞原代培养中I型和III型胶原合成的刺激作用。在允许最大刺激的浓度下,成纤维细胞培养通过增加胶原分泌来响应该剂,但与I型相比,III型的程度较低,导致I/III型胶原比例增加。我们发现,AA对I型和III型胶原分泌的刺激随着供体年龄的增长呈显著的线性下降(斜率= 1.9;P = 0.0014,斜率= -0.5;P = 0.0164)。我们还观察到年龄相关的AA对I型胶原细胞相关胶原池的刺激,但对III型胶原没有(斜率= 0.29;P = 0.015)。这可能表明成纤维细胞分泌新合成的I型胶原的能力降低与细胞对AA刺激的反应丧失有关。AA刺激对身体部位的作用分析表明,随着年龄的增长,耳周的I型和III型胶原合成的AA刺激损失更多(斜率= 2.7;P = 0.0280,斜率= -0.8;P = 0.0309)比乳腺皮肤(斜率= 2.1;P = 0.0071,斜率= 0.1;P = 0.7337)。这使我们考虑暴露在紫外线下的皮肤部位对AA的反应可能加速细胞真皮老化,使该参数成为人类真皮细胞老化的定量指标。
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Age-related response of human dermal fibroblasts to L-ascorbic acid: study of type I and III collagen synthesis.

Stimulation of the synthesis of type I and III collagens by 0.15 mM L-ascorbic acid (AA) was investigated in primary cultures of dermal fibroblasts form 30 females aged between 19 and 70 years. At this concentration allowing maximal stimulation, fibroblast cultures responded to this agent by an increase in collagen secretion, but to a lower extent for type III compared to type I, leading to an increase in the type I/III collagen ratio. We showed that AA stimulation of type I and III collagen secretion decreased in a statistically significant linear manner with donor age (slope = 1.9; p = 0.0014 and slope = -0.5; p = 0.0164, respectively). We also observed an age-related AA stimulation of the cell-associated collagen pool for type I collagen but not for type III (slope = 0.29; p = 0.015). This might indicate that a reduced ability of fibroblasts to secrete the newly synthesized type I collagen is involved in loss of the cellular response to AA stimulation. Analysis of AA stimulation as a function of body site showed that during aging, the loss of AA stimulation of type I and III collagen synthesis was more for periauricular (slope = 2.7; p = 0.0280 and slope = -0.8; p = 0.0309, respectively) than for mammary skin (slope = 2.1; p = 0.0071 and slope = 0.1; p = 0.7337, respectively). This led us to consider that UV-exposed cutaneous sites may accelerate cellular dermal aging in terms of response to AA, making this parameter a quantitative indicator of human dermal cell aging.

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