经肿瘤坏死因子-α处理的人脂肪来源干细胞可增强固有辐射耐受性,缓解体内辐射诱发的囊性挛缩。

Chanutchamon Sutthiwanjampa, Seung Hyun Kang, Mi Kyung Kim, Jin Hwa Choi, Han Koo Kim, Soo Hyun Woo, Tae Hui Bae, Woo Joo Kim, Shin Hyuk Kang, Hansoo Park
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引用次数: 0

摘要

导言:乳房切除术后放疗在乳腺癌治疗中起着至关重要的作用,但可能导致炎症反应,造成软组织损伤,特别是辐射诱发的囊性挛缩(RICC),影响乳房重建的效果。众所周知,脂肪源性干细胞(ADSCs)通过旁分泌能力具有再生潜力,并表现出固有的辐射耐受性。据报道,肿瘤坏死因子-α(TNF-α)对 ADSCs 的影响可增强 ADSCs 的旁分泌效应,通过调节炎症反应促进伤口愈合:本研究探讨了硅胶植入物上经TNF-α处理的人ADSCs(T-hASCs)缓解RICC的潜力,假设通过调节辐射暴露环境中的炎症反应来增强对RICC的抑制作用:方法:在体外,T-hASCs 被培养在不同的表面,以评估暴露于 20 Gy 辐射后的存活率。在体内,将T-hASC和未经TNF-α处理的hASC(C-hASCs)涂膜在辐射前植入小鼠体内,并在植入4周和8周后评估RICC的缓解情况。此外,还对T-hASCs释放的生长因子进行了评估:结果:在体外,hASCs表现出明显的辐射耐受性,在暴露于10 Gy辐射后仍能保持稳定的存活率。TNF-α处理进一步增强了辐射耐受性,在20 Gy时,其存活率明显高于C-hASCs。在体内,涂有T-hASC的植入物能有效抑制RICC,减少囊的厚度。T-hASCs 对炎症反应有明显的调节作用,抑制了巨噬细胞的 M1 极化,同时增强了巨噬细胞的 M2 极化。T-hASCs分泌的血管内皮生长因子被认为可诱导巨噬细胞极化,从而减少RICC:这项研究证实,T-hASCs 是一种很有前景的策略,可改善乳房切除术和放疗后乳房重建患者的不良反应。观察到的放射耐受性、抗纤维化作用和免疫调节功能表明,T-hASCs 有可能提高患者的治疗效果和生活质量。为了更广泛的临床应用,还需要进一步的研究和临床试验。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Tumor necrosis factor-α-treated human adipose-derived stem cells enhance inherent radiation tolerance and alleviate in vivo radiation-induced capsular contracture.

Introduction: Post-mastectomy radiotherapy plays a crucial role in breast cancer treatment but can lead to an inflammatory response causing soft tissue damage, particularly radiation-induced capsular contracture (RICC), impacting breast reconstruction outcomes. Adipose-derived stem cells (ADSCs), known for their regenerative potential via paracrine capacity, exhibit inherent radiotolerance. The influence of tumor necrosis factor-alpha (TNF-α) on ADSCs has been reported to enhance the paracrine effect of ADSCs, promoting wound healing by modulating inflammatory responses.

Objective: This study investigates the potential of TNF-α-treated human ADSCs (T-hASCs) on silicone implants to alleviate RICC, hypothesizing to enhance suppressive effects on RICC by modulating inflammatory responses in a radiation-exposed environment.

Methods: In vitro, T-hASCs were cultured on various surfaces to assess viability after exposure to radiation up to 20 Gy. In vivo, T-hASC and non-TNF-α-treated hASC (C-hASCs)-coated membranes were implanted in mice before radiation exposure, and an evaluation of the RICC mitigation took place 4 and 8 weeks after implantation. In addition, the growth factors released from T-hASCs were assessed.

Results: In vitro, hASCs displayed significant radiotolerance, maintaining consistent viability after exposure to 10 Gy. TNF-α treatment further enhanced radiation tolerance, as evidenced by significantly higher viability than C-hASCs at 20 Gy. In vivo, T-hASC-coated implants effectively suppressed RICC, reducing capsule thickness. T-hASCs exhibited remarkable modulation of the inflammatory response, suppressing M1 macrophage polarization while enhancing M2 polarization. The elevated secretion of vascular endothelial growth factor from T-hASCs is believed to induce macrophage polarization, potentially reducing RICC.

Conclusion: This study establishes T-hASCs as a promising strategy for ameliorating the adverse effects experienced by breast reconstruction patients after mastectomy and radiation therapy. The observed radiotolerance, anti-fibrotic effects, and immune modulation suggest the possibility of enhancing patient outcomes and quality of life. Further research and clinical trials are warranted for broader clinical uses.

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