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首页> 外文期刊>Journal of Pathology: Journal of the Pathological Society of Great Britain and Ireland >The fibrotic phenotype of systemic sclerosis fibroblasts varies with disease duration and severity of skin involvement: reconstitution of skin fibrosis development using a tissue engineering approach.
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The fibrotic phenotype of systemic sclerosis fibroblasts varies with disease duration and severity of skin involvement: reconstitution of skin fibrosis development using a tissue engineering approach.

机译：全身性硬化症成纤维细胞的纤维化表型随疾病持续时间和皮肤受累程度而异：使用组织工程学方法重建皮肤纤维化发展。

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摘要

We set out to examine the pathophysiological mechanisms of fibrosis in diffuse systemic sclerosis (SSc) using a tissue engineering approach. Skin fibroblasts were isolated from lesional skin of SSc patients with a disease duration of less than 1 year (early-stage SSc) or more than 10 years (late-stage SSc). Fibroblasts were also isolated from non-lesional skin and compared with normal fibroblasts isolated from healthy adults. Cells were cultured using a tissue engineering method to reconstruct a human dermis, and histologically observed. Dermal thickness was measured, as it reflects the global and intrinsic capacity of cells to reconstitute matrix. Collagen I, MMP-1, and MMP activity were evaluated. Cells were treated with TGFbeta1 or CTGF during dermis formation to study their fibrogenic role. Clinical severity of skin involvement was measured by a modified Rodnan score. Thickness of the dermis generated with non-lesional early-stage SSc fibroblasts was similar to normal cells. In contrast, reconstructed dermis from lesional early-stage SSc fibroblasts and non-lesional late-stage SSc cells was thinner, while lesional late-stage SSc fibroblasts made a thicker dermis. Dermis was always thicker when produced with TGFbeta1-treated cells, except when lesional late-stage SSc fibroblasts from patients with high Rodnan skin scores were used. CTGF did not affect dermal thickness. Measurements of collagen I and collagenases in the culture medium of the various reconstructed dermis could explain some of the changes observed. We conclude that the fibrotic phenotype of SSc fibroblasts varies with disease duration and with severity of skin involvement, and this is clearly visualized during in vitro dermis reconstruction.
机译：我们开始使用组织工程学方法检查弥漫性全身性硬化症（SSc）中纤维化的病理生理机制。从病程少于1年（早期SSc）或超过10年（晚期SSc）的SSc患者的病变皮肤中分离出皮肤成纤维细胞。还从非病变皮肤中分离出成纤维细胞，并将其与从健康成年人中分离出的正常成纤维细胞进行比较。使用组织工程方法培养细胞以重建人真皮，并进行组织学观察。测量皮肤厚度，因为它反映了细胞重构基质的整体能力和内在能力。评估胶原蛋白I，MMP-1和MMP活性。在真皮形成过程中，用TGFbeta1或CTGF处理细胞以研究其纤维化作用。皮肤受累的临床严重程度通过改良的Rodnan评分来衡量。非损伤性早期SSc成纤维细胞产生的真皮厚度与正常细胞相似。相反，从病变早期SSc成纤维细胞和非病变晚期SSc细胞重建的真皮较薄，而病变后期SSc成纤维细胞则真皮更厚。用TGFbeta1处理的细胞生产时，真皮总是较厚，除非使用了来自Rodnan皮肤评分高的患者的病变晚期SSc成纤维细胞。 CTGF不会影响真皮厚度。在各种重建的真皮培养基中测量胶原蛋白I和胶原酶可以解释所观察到的某些变化。我们得出结论，SSc成纤维细胞的纤维化表型随疾病持续时间和皮肤受累程度而变化，并且在体外真皮重建过程中可以清楚地看到这一点。

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