Iwata Takeo, Kuwajima Masamichi, Sukeno Akiko, Ishimaru Naozumi, Hayashi Yoshio, Wabitsch Martin, Mizusawa Noriko, Itakura Mitsuo, Yoshimoto Katsuhiko
Department of Medical Pharmacology, Institute of Health Biosciences, The University of Tokushima Graduate School, Tokushima 770-8504, Japan.
Biochem Biophys Res Commun. 2009 Oct 23;388(3):511-6. doi: 10.1016/j.bbrc.2009.08.024. Epub 2009 Aug 8.
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.
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一个来源。我们将YKL-40鉴定为人类内脏AT中SVF细胞分泌的一种主要蛋白质。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仅在内脏AT的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，并提高I型胶原的纤维形成速率。前脂肪细胞与巨噬细胞之间的相互作用增强了前脂肪细胞和巨噬细胞中MMP-1的表达。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。
