Author: Lien, Gi-Shih; Liu, Jen-Fang; Chien, Ming-Hsien; Hsu, Wei-Tse; Chang, Tzu-Hao; Ku, Chia-Chi; Ji, Andrea Tung-Qian; Tan, Peng; Hsieh, Ting-Lieh; Lee, Liang-Ming; Ho, Jennifer H
Title: The ability to suppress macrophage-mediated inflammation in orbital fat stem cells is controlled by miR-671-5p Document date: 2014_8_13
ID: 1i6hni9s_44
Snippet: We first report that endogenous miR-671-5p participates in immunomodulation of MSCs by directly targeting sTNFR type II and IL-1RA, which are two inhibitory molecules. In this study, we find that LPS triggers the proinflammatory ability of macrophages (Figures 1, 3 A and 7A), while OFSCs inhibit the proinflammatory activities (Figures 1, 3 and 7B) and induce cell cycle arrest ( Figure 2 ) in macrophages through the paracrine effect. LPS-activated.....
Document: We first report that endogenous miR-671-5p participates in immunomodulation of MSCs by directly targeting sTNFR type II and IL-1RA, which are two inhibitory molecules. In this study, we find that LPS triggers the proinflammatory ability of macrophages (Figures 1, 3 A and 7A), while OFSCs inhibit the proinflammatory activities (Figures 1, 3 and 7B) and induce cell cycle arrest ( Figure 2 ) in macrophages through the paracrine effect. LPS-activated macrophages excite the immunomodulatory capacity of OFSCs via upregulation of IDO, IL-10, sTNFR type II and IL-1RA (Figures 4 and 7B,C) . Among these factors, sTNFR type II and IL-1RA in OFSCs are negatively regulated by miR-671-5p under normal conditions ( Figures 5 and 7A) , and can be rapidly upregulated by degradation of miR-671-5p in OFSCs triggered by activated macrophages (Figures 4, 5 and 7B) , which enhances the anti-inflammatory ability of OFSCs (Figures 6 and 7C ). According to our data, the condition medium from OFSCs significantly reduced the proliferation and proinflammatory ability in macrophages (Figures 1, 2 and 3) , and the immunomodulatory ability of OFSCs could be induced by noncontact culture with LPS-activated macrophages (Figure 4) , indicating that paracrine effects of OFSCs play an important role in macrophage regulation. In addition, the therapeutic potency of OFSCs for attenuating macrophage-mediated inflammation was stronger ( Figure 1B ) than inducing macrophage cell cycle arrest (Figure 2A) . It is known that the number ratio of MSCs versus immune cells is critical for the therapeutic effect of immunomodulation in MSCs regulating lymphocytes (MSC/lymphocyte ratio > 0.1) [6, 31, 32] or natural killer cells (MSC/natural killer cells from 0.1 to 1) [15, 33] . We demonstrated that a ratio of OFSCs versus macrophages ≥1 (Figures 1B and 3) initiates anti-inflammation, while a ratio ≥2 initiates induction of macrophage cell cycle arrest (Figure 2) .
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