Abstract

<p class="AbstractContent"><strong>Objective</strong>: Temporomandibular joint (TMJ) arthritis can be induced by several inflammatory cytokines that may affect extracellular matrix (ECM) component expression. Link-N is exfoliated from Link protein (LP) which is one of the ECM components. It possesses ability to stimulate synthesis of ECM component. However, information regarding the potential of Link-N to modulate inflammatory process remains lacking.</p><p class="AbstractContent"><strong>Methods:</strong> Mesenchymal stem cells (MSCs) derived from oral adipose tissues were isolated from dental operation under regulation of IRB, and were stained by the early stage stem cell markers (OCT4, NANOG, REX1, and SOX2). MSCs were under IL-1β (1ng/ml) or Link-N (1μg/ml) stimulation at 24 hours and 96 hours. Cell supernatant were collected then concentration quantification of cytokines was performed by Luminex multiplex assays.</p><p class="AbstractContent"><strong>Results</strong>: MSCs showed the early stage stem cell markers. IP-10 and IL-6 increased significantly under IL-1βstimulation, but Link-N did not. The protection marker, IL-4, IL-13 elevated during Link-N treatment compared with only IL-1β stimulation at 24, 96 hours. The chondrogenesis regulator, TGF-β, increased significantly compared with only IL-1β stimulation at 96 hours.</p><p class="AbstractContent"><strong>Conclusion:</strong> During inflammation, Link-N can inhibit inflammatory response. On the other hand, it can enhance protection marker and chondrogenesis regulator expression. Link N may provide additional effect to assist joint repair.</p>

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