YKL-40 secreted from adipose tissue inhibits degradation of type I collagen
YKL-40 secreted from adipose tissue inhibits degradation of type I collagen
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DOI：
10.1016/j.bbrc.2009.08.024
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发表时间：
2009-10-23
影响因子：
3.1
通讯作者：
Yoshimoto, Katsuhiko
中科院分区：
文献类型：
--
作者：
Iwata, Takeo;Kuwajima, Masamichi;Yoshimoto, Katsuhiko
肥胖被认为是一种慢性低度炎症状态，脂肪组织 (AT) 的基质血管成分 (SVF) 细胞被认为是炎症相关分子的来源。我们确定 YKL-40 是人内脏 AT 中 SVF 细胞分泌的主要蛋白质。内脏 AT 的 SVF 细胞中 YKL-40 的表达水平高于皮下 AT 的 SVF 细胞。免疫荧光染色显示YKL-40仅在SVF细胞中的巨噬细胞中表达。从 SVF 细胞中纯化的 YKL-40 可抑制基质金属蛋白酶 (MMP)-1 对 AT 的主要细胞外基质 I 型胶原的降解，并增加 I 型胶原纤维形成的速率。前脂肪细胞和巨噬细胞中 MMP-1 的表达因这些细胞之间的相互作用而增强。这些结果表明，巨噬细胞/前脂肪细胞相互作用增强了AT中I型胶原的降解，同时，浸润到AT中的巨噬细胞分泌的YKL-40抑制了I型胶原的降解。 (C) 2009 Elsevier Inc. 保留所有权利。
Obesity is considered a chronic low-grade inflammatory status and the stromal vascular fraction (SVF) cells of adipose tissue ( AT) are considered a source of inflammation-related molecules. We identified YKL-40 as a major protein secreted from SVF cells in human visceral AT. YKL-40 expression levels in SVF cells from visceral AT were higher than in those from subcutaneous AT. Immunofluorescence staining revealed that YKL-40 was exclusively expressed in macrophages among SVF cells. YKL-40 purified from SVF cells inhibited the degradation of type I collagen, a major extracellular matrix of AT, by matrix metalloproteinase (MMP)-1 and increased rate of fibril formation of type I collagen. The expression of MMP-1 in preadipocytes and macrophages was enhanced by interaction between these cells. These results suggest that macrophage/preadipocyte interaction enhances degradation of type I collagen in AT, meanwhile, YKL-40 secreted from macrophages infiltrating into AT inhibits the type I collagen degradation. (C) 2009 Elsevier Inc. All rights reserved.