2026-03-05T08:02:25Z https://tokushima-u.repo.nii.ac.jp/oai

oai:tokushima-u.repo.nii.ac.jp:02002883 2025-04-28T06:32:49Z 1713853213384:1713853295607

YKL-40 secreted from adipose tissue inhibits degradation of type I collagen 岩田, 武男 1264 イワタ, タケオ 10350399 Iwata, Takeo クワジマ, マサミチ クワジマ, マサミチ Kuwajima, Masamichi スケノ, アキコ スケノ, アキコ Sukeno, Akiko 石丸, 直澄 1721 イシマル, ナオズミ 60444/profile-ja.html Ishimaru, Naozumi 60314879 林, 良夫 1659 ハヤシ, ヨシオ 60321/profile-ja.html Hayashi, Yoshio 00127854 Wabitsch, Martin 水澤, 典子 1255 ミズサワ, ノリコ 82856/profile-ja.html Mizusawa, Noriko 80254746 板倉, 光夫 174 イタクラ, ミツオ 10969/profile-ja.html Itakura, Mitsuo 60134227 吉本, 勝彦 1648 ヨシモト, カツヒコ 60308/profile-ja.html Yoshimoto, Katsuhiko 90201863 YKL-40 MMP-1 type I collagen adipose tissue macrophage preadipocyte 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. journal article 2009-10-23 AM application/pdf Biochemical and Biophysical Research Communications 3 388 511 516 0006291X AA00564395 https://tokushima-u.repo.nii.ac.jp/record/2002883/files/LID201602262002.pdf https://tokushima-u.repo.nii.ac.jp/records/2002883 eng © 2009 Elsevier Inc. All rights reserved.© 2009. This manuscript version is made available under the CC-BY-NC-ND 4.0 license