AIMS The present study aimed to explore the effect of syndecan-1 on keloid fibroblasts. MAIN METHODS Immunohistochemistry and Western blot were employed to assess the expression of syndecan-1. Primary cultured keloid fibroblasts were transfected with syndecan-1 siRNA. The function of syndecan-1 on the proliferation of keloid fibroblasts was investigated through Cell Counting Kit-8 (CCK-8) and flow cytometry. Extracellular matrix, TGF-β1/Smad, and MAPK related proteins were evaluated by Western blot. KEY FINDINGS Syndecan-1 was significantly overexpressed in both keloid tissues and fibroblasts. Moreover, the knockdown of syndecan-1 remarkably attenuated the proliferation of keloid fibroblasts and reduced the content of the extracellular matrix. Importantly, syndecan-1 regulates the expression of the extracellular matrix in keloid fibroblasts via TGF-β1/Smad and mitogen-activated protein kinase (MAPK) signaling pathways. SIGNIFICANCE The current results revealed a crucial function for syndecan-1 in regulating the expression of extracellular matrix and cell proliferation, thereby designating syndecan-1 as a novel target for keloid.

中文翻译：

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Syndecan-1通过TGF-β1/ Smad和MAPK信号通路调节瘢痕loid成纤维细胞中细胞外基质的表达。

目的本研究旨在探讨syndecan-1对瘢痕loid成纤维细胞的作用。主要方法采用免疫组化和Western blot评估syndecan-1的表达。用syndecan-1 siRNA转染原代培养的瘢痕loid成纤维细胞。通过细胞计数试剂盒8（CCK-8）和流式细胞仪研究了syndecan-1对瘢痕loid成纤维细胞增殖的功能。通过蛋白质印迹法评估细胞外基质，TGF-β1/ Smad和MAPK相关蛋白。主要发现Syndecan-1在瘢痕loid组织和成纤维细胞中均明显过表达。此外，syndecan-1的敲除显着减弱了瘢痕loid成纤维细胞的增殖并降低了细胞外基质的含量。重要的，syndecan-1通过TGF-β1/ Smad和有丝分裂原激活的蛋白激酶（MAPK）信号通路调节瘢痕loid成纤维细胞中细胞外基质的表达。意义目前的结果表明，syndecan-1在调节细胞外基质的表达和细胞增殖中起着至关重要的作用，从而将syndecan-1指定为瘢痕loid的新靶标。