Low‑intensity pulsed ultrasound promotes periodontal ligament stem cell migration through TWIST1‑mediated SDF‑1 expression.

Low‑intensity pulsed ultrasound promotes periodontal ligament stem cell migration through TWIST1‑mediated SDF‑1 expression.
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低强度脉冲超声通过TWIST1介导的SDF-1表达促进牙周膜干细胞迁移

DOI:
10.3892/ijmm.2018.3592
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发表时间:
2018-07
影响因子:
5.4
通讯作者:
Song J
Song J
中科院分区:
医学3区
文献类型:
--
作者:
Wang Y;Li J;Qiu Y;Hu B;Chen J;Fu T;Zhou P;Song J

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低强度脉冲超声(LIPUS)是一种非侵入性的治疗方法,可加速骨折愈合。我们小组以前的一项研究表明,LIPUS具有促进牙周组织再生的潜力。然而,LIPUS促进牙周组织再生的潜在分子机制仍然未知。本研究从前磨牙中分离牙周膜干细胞。流式细胞术和分化测定用于表征分离的PDLSC。对PDLSC进行LIPUS处理,并通过逆转录-定量聚合酶链反应检测基质细胞衍生因子-1(SDF-1)表达水平,使用或不使用AMD 3100阻断SDF-1/C-X-C基序趋化因子受体4(CXCR 4)通路。ELISA用于评估PDLSC中SDF-1的分泌。进行伤口愈合和transwell测定以评估LIPUS的促进迁移作用。SDF-1的一个潜在的上游基因twist家族bHLH转录因子1(TWIST 1)通过小干扰(si)RNA转染被沉默。结果表明,LIPUS处理促进TWIST 1和SDF-1在mRNA和蛋白水平的表达。此外,LIPUS处理增强PDLSC的细胞迁移。TWIST 1的敲低可损害PDLSCs的SDF-1表达和细胞迁移能力。TWIST 1可能是PDLSC中SDF-1的上游调节因子。综上所述,这些结果表明,SDF 1/CXCR 4信号通路参与了LIPUS促进PDLSC迁移,这可能是LIPUS介导的牙周再生的机制之一。TWIST 1可能是机械力传导过程中的机械应力传感器。
Low-intensity pulsed ultrasound (LIPUS) is a non-invasive therapeutic treatment for accelerating fracture healing. A previous study from our group demonstrated that LIPUS has the potential to promote periodontal tissue regeneration. However, the underlying molecular mechanism by which LIPUS promotes periodontal tissue regeneration remains unknown. In the present study, periodontal ligament stem cells (PDLSCs) were isolated from premolars. Flow cytometry and differentiation assays were used to characterize the isolated PDLSCs. LIPUS treatment was administered to PDLSCs, and stromal cell-derived factor-1 (SDF-1) expression levels were examined by reverse transcription-quantitative polymerase chain reaction with or without blocking the SDF-1/C-X-C motif chemokine receptor 4 (CXCR4) pathway with AMD3100. ELISA was used to evaluate SDF-1 secretion in PDLSCs. Wound healing and transwell assays were conducted to assess the migration-promoting effect of LIPUS. A potential upstream gene of SDF-1, twist family bHLH transcription factor 1 (TWIST1), was silenced by small interfering (si) RNA transfection. The results demonstrated that LIPUS treatment promoted the expression of TWIST1 and SDF-1 at both the mRNA and protein levels. In addition, LIPUS treatment enhanced the cell migration of PDLSCs. Knockdown of TWIST1 impaired the expression of SDF-1 and the cell migration ability of PDLSCs. TWIST1 may be an upstream regulator of SDF-1 in PDLSCs. Taken together, these findings indicate that the SDF1/CXCR4 signaling pathway is involved in LIPUS-promoted PDLSC migration, which might be one of the mechanisms for LIPUS-mediated periodontal regeneration. TWIST1 might be a mechanical stress sensor during mechanotransduction.
DOI: 10.18632/oncotarget.13890
发表时间: 2017-01-31
期刊: Oncotarget
影响因子: --
作者:
Duan Y;He Q;Yue K;Si H;Wang J;Zhou X;Wang X
通讯作者: Wang X
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期刊: PloS one
影响因子: 3.7
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