Tumour necrosis factor-alpha but not Interleukin-1-beta inhibits uniaxial cyclic strain induced tenogenic differentiation of human mesenchymal stromal cells in vitro

IF 2.5 4区生物学 Q1 ANATOMY & MORPHOLOGY

Tissue & cell Pub Date : 2025-06-14 DOI:10.1016/j.tice.2025.103018

Shaliny Krishnan , Hui Yin Nam , Amirah Zulkifli , Peggy Kong , Cheh Chin Tai , Azura Mansor , Tunku Kamarul

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引用次数: 0

Abstract

Uniaxial cyclic strain induces tenogenic differentiation of mesenchymal stromal cells (MSCs), suggesting its beneficial role in tendon regeneration following injury. However, pro-inflammatory cytokines released during injury is expected to impede repair outcomes but has not been previously considered. A study was thus conducted to determine the effects of interleukin-1-beta (IL-1β) and tumour necrosis factor-alpha (TNF-α) on the tenogenic differentiation potential of cyclic strained MSCs. An in vitro model of MSCs exposed to IL-1β (9 ng/ml) and TNF-α (6 ng/ml) in unstrained and strained conditions, were developed. The effect of these cytokines on MSCs functional properties including proliferation, viability, anabolic/catabolic protein production and tenogenic differentiation potential of MSCs were quantified. IL-1β (9 ng/ml) and TNF-α (6 ng/ml) reduced unstrained MSCs viability, proliferation, ECM protein production and tenogenic markers expression whilst increasing matrix metalloproteinase 13 (MMP-13) expression. Uniaxial strain exposure in IL-1β-treated MSCs reversed the inhibitory effects of this cytokine on cell proliferation, collagen production and tenogenic markers expression. The significant reduction in tenogenic potential observed in MSCs treated with TNF-α was not alleviated by cyclic strain. These data indicate that TNF-α and not IL-1β is able to inhibit tenogenic effects induced by uniaxial cyclic strain on MSCs.

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肿瘤坏死因子- α而非白细胞介素-1- β抑制单轴循环菌株诱导的人间充质间质细胞的体外成腱分化

单轴循环应变诱导间充质间质细胞（MSCs）成肌腱分化，提示其在损伤后肌腱再生中的有益作用。然而，损伤过程中释放的促炎细胞因子可能会阻碍修复结果，但此前并未考虑到这一点。因此，我们进行了一项研究，以确定白细胞介素-1- β (IL-1β)和肿瘤坏死因子-α (TNF-α)对环张力MSCs的成腱鞘分化潜能的影响。建立了IL-1β（9 ng/ml）和TNF-α（6 ng/ml）暴露于非应变和应变条件下的MSCs体外模型。量化这些细胞因子对MSCs功能特性的影响，包括增殖、活力、合成代谢/分解代谢蛋白的产生和MSCs的成肌腱分化潜力。IL-1β（9 ng/ml）和TNF-α（6 ng/ml）降低了未处理MSCs的活力、增殖、ECM蛋白的产生和肌腱生成标志物的表达，同时增加了基质金属蛋白酶13 （MMP-13）的表达。单轴菌株暴露于il -1β处理的MSCs中，逆转了该细胞因子对细胞增殖、胶原生成和肌腱生成标志物表达的抑制作用。TNF-α处理的MSCs的成腱电位明显降低，但循环应变并未减轻。这些数据表明，TNF-α而非IL-1β能够抑制单轴循环应变诱导的MSCs的成腱鞘效应。

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来源期刊

Tissue & cell 医学-解剖学与形态学

CiteScore

3.90

自引率

0.00%

发文量

234

期刊介绍： Tissue and Cell is devoted to original research on the organization of cells, subcellular and extracellular components at all levels, including the grouping and interrelations of cells in tissues and organs. The journal encourages submission of ultrastructural studies that provide novel insights into structure, function and physiology of cells and tissues, in health and disease. Bioengineering and stem cells studies focused on the description of morphological and/or histological data are also welcomed. Studies investigating the effect of compounds and/or substances on structure of cells and tissues are generally outside the scope of this journal. For consideration, studies should contain a clear rationale on the use of (a) given substance(s), have a compelling morphological and structural focus and present novel incremental findings from previous literature.