The ability to suppress macrophage-mediated inflammation in orbital fat stem cells is controlled by miR-671-5p

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

Finally, OFSCs with or without miR-671-5p inhibitor transfection were systemically injected into mice with LPS-induced ALI, and the therapeutic effect of both in the first 6 hours was compared. We measured the malondialdehyde level, a readout of lipid peroxidation, as the indicator of redox status in the lungs. The results showed that the redox status in a LPS-damaged lung parenchyma was significantly reduced by both OFSCs and OFSCs with preinhibition of miR-671-5p ( Figure 6A ). Tissue sections showed that LPS triggered the inflammatory cell infiltration into interstitial space of lung parenchyma, and increased lung permeability by fluid accumulation in alveolar space ( Figure 6B ). OFSC transplantation ameliorated lung permeability and inflammatory in the first 6 hours ( Figure 6C) . Moreover, less cell infiltration and larger alveolar space were noted in ALI mice receiving miR-671-5p-inhibited OFSCs compared with those mice receiving OFSCs ( Figure 6D ), demonstrating that preinhibition of miR-671-5p in OFSCs further enhanced the anti-inflammation ability in lung parenchyma without altering the antioxidative ability in OFSCs ( Figure 6A ).