Low-intensity pulsed ultrasound promotes osteoarthritic cartilage regeneration by BMSC-derived exosomes via modulating the NF-ΚB signaling pathway
Low-intensity pulsed ultrasound promotes osteoarthritic cartilage regeneration by BMSC-derived exosomes via modulating the NF-ΚB signaling pathway
复制标题
低强度脉冲超声通过调节 NF-κB 信号通路促进 BMSC 衍生的外泌体再生骨关节炎软骨
DOI：
10.1016/j.intimp.2021.107824
复制
发表时间：
2021-06-05
影响因子：
5.6
通讯作者：
Liu, Gang
中科院分区：
文献类型：
--
作者：
Liao, Qing;Li, Bao Jian;Liu, Gang
骨关节炎是世界范围内最常见的致残性关节疾病，临床治疗效果仍不理想。最近的研究表明，间充质干细胞（MSC）来源的外泌体可以促进骨关节炎的软骨修复和再生，表明这些外泌体可能是治疗骨关节炎的一种新的和有前途的策略。这项研究调查了低强度脉冲超声（LIPUS）是否增强了骨髓MSC（BMSC）衍生的外泌体对骨关节炎软骨再生的影响，并研究了潜在的机制。我们的研究结果表明，BMSC来源的exosomes显示了exosomes的典型形态特征。LIPUS介导的BMSC来源的外泌体促进软骨再生，增加软骨细胞增殖和细胞外基质合成，抑制炎症，并抑制白细胞介素（IL）-1 β诱导的核因子κ B（NF Kappa B）途径的激活。总之，LIPUS增强了BMSC来源的外泌体对骨关节炎软骨再生的促进作用，主要是通过加强炎症抑制作用，进一步增强软骨细胞增殖和软骨基质合成。其潜在机制可能与抑制IL-1 β诱导的NF-κ B通路活化有关。
Osteoarthritis is the most common disabling joint disease throughout the world, and the effect of therapy on its course is still unsatisfactory in clinical practice. Recent studies have shown that mesenchymal stem cell (MSC)derived exosomes can promote cartilage repair and regeneration in osteoarthritis, indicating that these exosomes could be a novel and promising strategy for treating osteoarthritis. This study investigated whether low-intensity pulsed ultrasound (LIPUS) enhances the effects of bone marrow MSC (BMSC)-derived exosomes on cartilage regeneration in osteoarthritis and examined the underlying mechanism. Our results revealed that BMSC-derived exosomes display the typical morphological features of exosomes. LIPUS-mediated BMSC-derived exosomes promoted cartilage regeneration, increased chondrocyte proliferation and extracellular matrix synthesis, suppressed inflammation, and inhibited the interleukin (IL)-1 beta-induced activation of the nuclear factor kappa B (NF Kappa B) pathway. In brief, LIPUS enhances the promoting effects of BMSC-derived exosomes on osteoarthritic cartilage regeneration, mainly by strengthening the inhibition of inflammation and further enhancing chondrocyte proliferation and cartilage matrix synthesis. The underlying mechanism could be related to the inhibition of the IL-1 beta-induced activation of the NF-Kappa B pathway.