Mechanobiology in Medicine最新文献_第4页

High-rate mechano-stimulation alters proliferation- and maturation-related signaling of oligodendrocyte precursor cells in a 3D hydrogel 高速率机械刺激改变了3D水凝胶中少突胶质前体细胞的增殖和成熟相关信号

Mechanobiology in Medicine

Pub Date : 2025-03-11 DOI: 10.1016/j.mbm.2025.100126

Ryosuke Yokosawa , Rachel A. Mazur , Kelsey A. Wilson , Jacob H. Lee , Noah W. Showalter , Kyle J. Lampe , Pamela J. VandeVord

Traumatic brain injury (TBI) leads to neuroinflammation and is associated with chronic neurodegeneration. Many TBI studies aim to understand further the mechanism by which cells in the brain respond to the mechanical forces associated with TBI. In particular, mild TBI is the most common level of injury among TBI patients, and the reactivity of glial cells is a key mechanism in understanding mild TBI. However, there is a lack of studies focusing on oligodendrocyte precursor cells (OPCs). OPCs respond to the injury by migration, proliferation, and differentiation into oligodendrocytes (OL) to assist in post-injury repair. Given their ability to proliferate and differentiate, OPCs are a promising therapeutic target for OL regeneration. Despite their important role in maintaining normal neuronal functions, the response of OPCs to mechanical insult remains poorly understood. Thus, this study aims to elucidate the cellular responses of OPCs using a brain-tissue mimicking in vitro 3D hydrogel platform to identify key signaling pathways driving their response. In this study, we applied a high-rate pressure wave to OPCs to induce mild TBI and assess subsequent cellular and molecular responses by quantifying cell growth, metabolic activity, and gene and protein expression. Although the high-rate mechanical insult did not significantly impact cell survival, it induced transcriptomic and proteomic changes in molecular targets related to OPC proliferation and maturation, including PDGFRA, GALC, CTNNB1, and HSP90AB. These dysregulations and altered molecular profiles provide valuable insights into the OPC injury response and may serve as potential therapeutic targets for treating neurodegeneration.

创伤性脑损伤（TBI）可导致神经炎症，并与慢性神经变性有关。许多TBI研究旨在进一步了解脑细胞对与TBI相关的机械力作出反应的机制。其中，轻度TBI是TBI患者中最常见的损伤级别，神经胶质细胞的反应性是理解轻度TBI的关键机制。然而，关于少突胶质前体细胞（OPCs）的研究却很少。OPCs通过迁移、增殖和分化成少突胶质细胞（OL）来响应损伤，以协助损伤后的修复。鉴于其增殖和分化的能力，OPCs是OL再生的一个有希望的治疗靶点。尽管OPCs在维持正常神经元功能方面发挥着重要作用，但对机械性损伤的反应仍然知之甚少。因此，本研究旨在利用一个模拟脑组织的体外3D水凝胶平台来阐明OPCs的细胞反应，以确定驱动其反应的关键信号通路。在这项研究中，我们对OPCs施加高速率压力波诱导轻度TBI，并通过量化细胞生长、代谢活性、基因和蛋白质表达来评估随后的细胞和分子反应。尽管高速率机械损伤没有显著影响细胞存活，但它诱导了与OPC增殖和成熟相关的分子靶点的转录组学和蛋白质组学变化，包括PDGFRA、GALC、CTNNB1和HSP90AB。这些失调和改变的分子谱为OPC损伤反应提供了有价值的见解，并可能作为治疗神经退行性疾病的潜在治疗靶点。

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引用次数: 0

Gut microbiota-derived butyrate enhances exercise-induced bone mineral density in humans 肠道微生物来源的丁酸盐增强人体运动诱导的骨密度

Mechanobiology in Medicine

Pub Date : 2025-03-05 DOI: 10.1016/j.mbm.2025.100124

Xiangya Dou , Pengyu Fu , Yuting Zhang , Yiwen Zhang , Kaiting Ning , Baoqiang Yang , Xuezhou Yang , Yinbo Niu , Dong-En Wang , Huiyun Xu

Bone Mineral Density (BMD) is one of the primary markers of bone health. Exercise provides constant mechanical stress to bone, which in turn increases BMD. Gut-bone axis is considered to play an important role in the regulation of exercise on bone. Also, the metabolites of gut microbiota (GM), especially short-chain fatty acids (SCFAs), are thought to be involved in the progress. In this study, by analyzing serum and GM from humans with low and high BMD, we found that exercise indeed enhanced BMD, and butyrate secreted from GM was involved in the regulation.

骨矿物质密度（BMD）是骨骼健康的主要指标之一。运动为骨骼提供持续的机械压力，从而增加骨密度。肠骨轴被认为在运动对骨骼的调节中起着重要作用。此外，肠道微生物群（GM）的代谢物，特别是短链脂肪酸（SCFAs），被认为参与了这一进程。本研究通过分析低骨密度和高骨密度人群的血清和GM，我们发现运动确实能提高骨密度，GM分泌的丁酸盐参与了调节。

引用次数: 0

Tropomodulin1 regulates the biomechanical changes in macrophages induced by matrix stiffness Tropomodulin1调节基质刚度诱导巨噬细胞的生物力学变化

Mechanobiology in Medicine

Pub Date : 2025-02-20 DOI: 10.1016/j.mbm.2025.100117

Yajun Meng , Amannisa Tuersuntuoheti , Siyu Jiang , Jiayi Xie , Zejun Yue , Dingwen Xu , Xueyu Geng , Xiang Lian , Lide Xie , Lanping Amy Sung , Xifu Wang , Jing Zhou , Weijuan Yao

The monocyte/macrophage infiltration plays critical roles in the development of atherosclerosis. Arterial stiffness is a cholesterol-independent risk factor for cardiovascular events. The regulation of arterial stiffness on biomechanics of macrophages and its underlying mechanism remains unclear. We prepared polyacrylamide gels with low and high stiffness that corresponded to healthy and diseased blood vessels, respectively. We found that macrophages cultured on stiff matrix had increased rigidity and migration ability compared to those on soft matrix. An actin capping protein, tropomodulin1 (Tmod1) was upregulated in macrophages by stiff matrix and in arteries with high stiffness. Further analyses showed that deficiency of Tmod1 in macrophages completely or partially prevented the changes in actin polymerization, cell adhesion and cell spreading induced by stiff matrix. Overexpression of Tmod1 in macrophages enhanced actin polymerization, cell adhesion and spreading on stiff matrix. Tmod1 was involved in the regulation of vinculin expression and formation of focal adhesion in macrophages on stiff matrix. Finally, the deficiency of Tmod1 in macrophages retarded the formation of atherosclerotic plaques in blood vessels with high matrix stiffness. The results suggest that Tmod1 was a key regulator in macrophage rigidity and migration on stiff substrate. The present work will help us to understand the biomechanical mechanisms for the development of atherosclerosis.

单核细胞/巨噬细胞浸润在动脉粥样硬化的发生发展中起关键作用。动脉僵硬是心血管事件的一个不依赖胆固醇的危险因素。动脉硬度对巨噬细胞生物力学的调节及其潜在机制尚不清楚。我们分别制备了与健康血管和病变血管相对应的低刚度和高刚度聚丙烯酰胺凝胶。我们发现在硬基质上培养的巨噬细胞比在软基质上培养的巨噬细胞具有更高的刚性和迁移能力。一种肌动蛋白封盖蛋白，tropomodulin1 （Tmod1）在巨噬细胞和高硬度动脉中被僵硬基质上调。进一步分析表明，巨噬细胞中Tmod1的缺失完全或部分阻止了硬基质诱导的肌动蛋白聚合、细胞粘附和细胞扩散的变化。巨噬细胞中过表达Tmod1可增强肌动蛋白聚合、细胞黏附和在坚硬基质上的扩散。Tmod1参与了巨噬细胞在刚性基质上表达和局灶黏附形成的调控。最后，巨噬细胞中缺乏Tmod1延缓了高基质刚度血管中动脉粥样硬化斑块的形成。结果表明，Tmod1是巨噬细胞刚性和在刚性底物上迁移的关键调节因子。本研究将有助于我们了解动脉粥样硬化发生的生物力学机制。

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引用次数: 0

Ultrasound imaging and regulated mechanotransduction for characteristics, regeneration, and therapeutics of bone 骨的特征、再生和治疗的超声成像和调节机械转导

Mechanobiology in Medicine

Pub Date : 2025-02-19 DOI: 10.1016/j.mbm.2025.100116

Yi-Xian Qin

Ultrasound imaging has been widely used in clinical diagnoses, such as B-mode and M-mode ultrasound imaging for cardiovascular, abdomen, OB-Gyn, and other soft tissue and organs in clinical diagnoses. Ultrasound imaging has traditionally been limited in its application to bone because of the high acoustic impedance and density of trabecular and cortical bone structure and density alterations, high wave reflection, absorption, scattering, and low penetration, which result in significant reflection and attenuation of ultrasonic energy in such mineral tissues. Recent advancements in quantitative ultrasound technology have opened new possibilities for noninvasive characteristics of bone quality through transmitted or backscattered signals, offering a radiation-free alternative to traditional imaging modalities like dual-energy X-ray absorptiometry (DEX), X-rays, and CT scans. In addition, low-intensity ultrasound (LIUS) has been studied and applied to promote bone regeneration and fracture healing through induced mechanotransduction in tissue and cells. The field of bone ultrasound encompasses fundamental research on the interaction of elastic waves with cortical and trabecular bone microstructures, the development of innovative imaging methodologies and medical applications such as bone health assessment for osteoporosis diagnosis, therapeutic use of LIUS, and phase aberration correction inside the skull. This work has highlighted recent developments and advancements in ultrasound diagnosis and therapeutics, induced cellular and molecular pathways, and future directions using ultrasound as a promising imaging tool and treatment method.

超声成像在临床诊断中得到了广泛的应用，如心血管、腹部、妇产科等软组织器官的b、m型超声成像在临床诊断中的应用。传统上，超声成像在骨中的应用受到限制，因为骨小梁和骨皮质结构的高声阻抗和密度以及密度改变，高波反射、吸收、散射和低穿透，导致超声能量在这类矿物组织中的反射和衰减明显。定量超声技术的最新进展为通过传输或后向散射信号检测骨质量的无创特征开辟了新的可能性，为双能x射线吸收仪（DEX）、x射线和CT扫描等传统成像方式提供了一种无辐射的替代方案。此外，低强度超声（LIUS）已被研究并应用于通过诱导组织和细胞的机械转导来促进骨再生和骨折愈合。骨超声领域包括弹性波与骨皮质和骨小梁微结构相互作用的基础研究，创新成像方法的发展和医学应用，如骨质疏松症诊断的骨健康评估，LIUS的治疗用途，以及颅骨内的相位像差校正。本文重点介绍了超声诊断和治疗、诱导细胞和分子途径的最新进展，以及超声作为一种有前途的成像工具和治疗方法的未来方向。

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引用次数: 0

Toward a clear relationship between mechanical signals and bone adaptation 研究机械信号与骨适应之间的关系

Mechanobiology in Medicine

Pub Date : 2025-02-01 DOI: 10.1016/j.mbm.2025.100115

Chenlu Wang, Ruisen Fu, Haisheng Yang

Bone adapts according to the mechanical environment, and this adaptation can be visualized by altering its shape, size, and microarchitecture. Bone adaptation was recognized more than a century ago, with a description presented in The Law of Bone Remodeling. Furthermore, the conceptual model of “The Mechanostat” provides a quantitative relationship between the magnitude of bone tissue deformation (strain) and bone adaptive responses. However, upon maintaining a constant strain magnitude, various bone responses were observed experimentally under different loading parameters (e.g., frequency, rate, number of load cycles, rest insertion, and waveform). Nevertheless, the precise relationship between mechanical signals and bone adaptation remains unclear. Accordingly, we reviewed in vivo loading studies to determine the quantitative relationships between various mechanical signals and bone adaptive responses in various animal loading models. Additionally, we explored how these relationships are influenced by pathophysiological factors, such as age, sex, and estrogen deficiency. Moreover, mechanistic studies that consider cellular mechanical microenvironments to explain these quantitative relationships are discussed. A general formula that considers the bone adaptive response as a function of different loading parameters was proposed. This review may enhance our understanding of bone adaptation and offer guidance for clinicians to develop effective mechanotherapies to prevent bone loss.

骨骼根据机械环境进行适应，这种适应可以通过改变其形状、大小和微结构来可视化。骨适应早在一个多世纪前就已被认识到，并在《骨重塑法则》中进行了描述。此外，“the Mechanostat”的概念模型提供了骨组织变形（应变）大小与骨适应性反应之间的定量关系。然而，在保持恒定应变量级的情况下，在不同的加载参数（例如，频率、速率、加载周期数、rest插入和波形）下，实验观察到不同的骨响应。然而，机械信号和骨适应之间的确切关系仍不清楚。因此，我们回顾了体内加载研究，以确定各种动物加载模型中各种机械信号与骨适应反应之间的定量关系。此外，我们探讨了这些关系如何受到病理生理因素的影响，如年龄、性别和雌激素缺乏。此外，还讨论了考虑细胞力学微环境来解释这些定量关系的机制研究。提出了一个考虑骨自适应响应作为不同载荷参数函数的通用公式。这一综述可以提高我们对骨适应的认识，并为临床医生开发有效的机械疗法来预防骨质流失提供指导。

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引用次数: 0

Angiogenesis within atherosclerotic plaques: Mechanical regulation, molecular mechanism and clinical diagnosis 动脉粥样硬化斑块内血管生成：机械调控、分子机制和临床诊断

Mechanobiology in Medicine

Pub Date : 2025-02-01 DOI: 10.1016/j.mbm.2025.100114

Hanxiao Chen , Chengxiu Peng , Fei Fang , Yuhao Li , Xiaran Liu , Ying Hu , Guixue Wang , Xiaoheng Liu , Yang Shen

Atherosclerosis (AS) is a disease characterized by focal cholesterol accumulation and insoluble inflammation in arterial intima, leading to the formation of an atherosclerotic plaque consisting of lipids, cells, and fibrous matrix. The presence of plaque can restrict or obstruct blood flow, resulting in arterial stenosis and local mechanical microenvironment changes including flow shear stress, vascular matrix stiffness, and plaque structural stress. Neovascularization within the atherosclerotic plaque plays a crucial role in both plaque growth and destabilization, potentially leading to plaque rupture and fatal embolism. However, the exact interactions between neovessels and plaque remain unclear. In this review, we provide a comprehensive analysis of the origin of intraplaque neovessels, the contributing factors, underlying molecular mechanisms, and associated signaling pathways. We specifically emphasize the role of mechanical factors contributing to angiogenesis in atherosclerotic plaques. Additionally, we summarize the imaging techniques and therapeutic strategies for intraplaque neovessels to enhance our understanding of this field.

动脉粥样硬化（AS）是一种以动脉内膜局灶性胆固醇积累和不溶性炎症为特征的疾病，导致由脂质、细胞和纤维基质组成的动脉粥样硬化斑块的形成。斑块的存在会限制或阻碍血流，导致动脉狭窄和局部机械微环境的改变，包括血流剪切应力、血管基质刚度和斑块结构应力。动脉粥样硬化斑块内的新生血管在斑块生长和不稳定中起着至关重要的作用，可能导致斑块破裂和致命的栓塞。然而，新血管和斑块之间的确切相互作用尚不清楚。在这篇综述中，我们对斑块内新血管的起源、影响因素、潜在的分子机制和相关的信号通路进行了全面的分析。我们特别强调机械因素在动脉粥样硬化斑块血管生成中的作用。此外，我们总结了斑块内新血管的成像技术和治疗策略，以提高我们对这一领域的理解。

{"title":"Angiogenesis within atherosclerotic plaques: Mechanical regulation, molecular mechanism and clinical diagnosis","authors":"Hanxiao Chen , Chengxiu Peng , Fei Fang , Yuhao Li , Xiaran Liu , Ying Hu , Guixue Wang , Xiaoheng Liu , Yang Shen","doi":"10.1016/j.mbm.2025.100114","DOIUrl":"10.1016/j.mbm.2025.100114","url":null,"abstract":"<div><div>Atherosclerosis (AS) is a disease characterized by focal cholesterol accumulation and insoluble inflammation in arterial intima, leading to the formation of an atherosclerotic plaque consisting of lipids, cells, and fibrous matrix. The presence of plaque can restrict or obstruct blood flow, resulting in arterial stenosis and local mechanical microenvironment changes including flow shear stress, vascular matrix stiffness, and plaque structural stress. Neovascularization within the atherosclerotic plaque plays a crucial role in both plaque growth and destabilization, potentially leading to plaque rupture and fatal embolism. However, the exact interactions between neovessels and plaque remain unclear. In this review, we provide a comprehensive analysis of the origin of intraplaque neovessels, the contributing factors, underlying molecular mechanisms, and associated signaling pathways. We specifically emphasize the role of mechanical factors contributing to angiogenesis in atherosclerotic plaques. Additionally, we summarize the imaging techniques and therapeutic strategies for intraplaque neovessels to enhance our understanding of this field.</div></div>","PeriodicalId":100900,"journal":{"name":"Mechanobiology in Medicine","volume":"3 1","pages":"Article 100114"},"PeriodicalIF":0.0,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143428126","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The underlying difference of metastatic and non-metastatic breast cancer cells in configuring type I collagen fibres to promote migration by cell mechanics 转移性和非转移性乳腺癌细胞在配置I型胶原纤维通过细胞力学促进迁移方面的潜在差异

Mechanobiology in Medicine

Pub Date : 2025-01-31 DOI: 10.1016/j.mbm.2025.100113

Mingxing Ouyang , Weihui Chen , Ting Zhou , Hongjie Liu , Lei Liu , Bing Bu , Linhong Deng

The progression of tumors is heavily influenced by mechanical properties of their microenvironment. In this work, we applied micropatterned models with varying distances and shapes to investigate the differences between metastatic MDA-MB-231 and non-metastatic MCF-7 breast cancer cells in reconfiguring extracellular matrix to promote cell migration induced by cell mechanics. Both cancer cells were able to rearrange type I collagen (COL) to form fibre threads, in which MDA-MB-231 consistently migrated more rapidly than MCF-7, ranging from geometrical square arrays with different spacings to complex polygonal models. MDA-MB-231 displayed higher capability of reorganizing fibre bundles at longer distance (800 μm). Further looking for differences in cell molecular mechanisms, siRNA knockdown inhibiting either integrin β1 or Piezo1 decreased fibre assembly and reduced the difference in COL remodeling and migration between two cancer cells. MDA-MB-231 showed inhibited migration with integrin knockdown, whereas scattering migration with Piezo1 knockdown, indicating cells losing directional mechanosensation. After inhibiting junctional E-cadherin with siRNA, MCF-7 cells migrated faster, resulting in reduced difference in comparison to MDA-MB-231 that didn't express E-cadherin. In summary, this work has explored the biomechanical differences between metastatic and non-metastatic breast cancer cells regarding COL fibre matrix remodeling and cell movements. The significant differences in E-cadherin expression in the two breast cancer cells had an effect on cell migrations. The results of this study provide research approaches for evaluating therapeutic effort on breast cancer.

肿瘤的发展在很大程度上受其微环境的力学特性的影响。在这项工作中，我们应用不同距离和形状的微图案模型来研究转移性MDA-MB-231和非转移性MCF-7乳腺癌细胞在细胞力学诱导的细胞外基质重新配置促进细胞迁移方面的差异。两种癌细胞都能够重新排列I型胶原蛋白（COL），形成纤维线，其中MDA-MB-231始终比MCF-7更快地迁移，范围从具有不同间距的几何方形阵列到复杂的多边形模型。MDA-MB-231在较远距离（800 μm）表现出较高的纤维束重组能力。进一步寻找细胞分子机制的差异，siRNA敲低抑制整合素β1或Piezo1减少了纤维组装，减少了两个癌细胞之间COL重塑和迁移的差异。MDA-MB-231在整合素敲低的情况下表现出被抑制的迁移，而在Piezo1敲低的情况下表现出散射迁移，表明细胞失去了定向机械感觉。用siRNA抑制连接E-cadherin后，MCF-7细胞迁移速度加快，与不表达E-cadherin的MDA-MB-231相比差异减小。总之，这项工作探讨了转移性和非转移性乳腺癌细胞在冷纤维基质重塑和细胞运动方面的生物力学差异。两种乳腺癌细胞中E-cadherin表达的显著差异对细胞迁移有影响。本研究结果为评价乳腺癌治疗效果提供了研究途径。

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引用次数: 0

Mechanotransduction and inflammation: An updated comprehensive representation 机械转导和炎症：更新的综合表征

Mechanobiology in Medicine

Pub Date : 2024-12-14 DOI: 10.1016/j.mbm.2024.100112

Vennila Suriyagandhi , Ying Ma , Veronica Paparozzi , Tiziana Guarnieri , Biagio Di Pietro , Giovanna Maria Dimitri , Paolo Tieri , Claudia Sala , Darong Lai , Christine Nardini

Mechanotransduction is the process that enables the conversion of mechanical cues into biochemical signaling. While all our cells are well known to be sensitive to such stimuli, the details of the systemic interaction between mechanical input and inflammation are not well integrated. Often, indeed, they are considered and studied in relatively compartmentalized areas, and we therefore argue here that to understand the relationship of mechanical stimuli with inflammation – with a high translational potential - it is crucial to offer and analyze a unified view of mechanotransduction. We therefore present here pathway representation, recollected with the standard systems biology markup language (SBML) and explored with network biology approaches, offering RAC1 as an exemplar and emerging molecule with potential for medical translation.

机械转导是将机械信号转化为生化信号的过程。虽然我们所有的细胞都对这些刺激敏感，但机械输入和炎症之间的系统相互作用的细节并没有很好地整合。事实上，它们通常是在相对分隔的领域被考虑和研究的，因此我们在这里认为，要理解机械刺激与炎症的关系-具有很高的转化潜力-提供和分析机械转导的统一观点至关重要。因此，我们在这里提出了途径表示，用标准系统生物学标记语言（SBML）进行了回忆，并用网络生物学方法进行了探索，提供了RAC1作为一个范例和具有医学翻译潜力的新兴分子。

引用次数: 0

Matrix stiffness and viscoelasticity influence human mesenchymal stem cell immunomodulation 基质刚度和粘弹性影响人间充质干细胞的免疫调节

Mechanobiology in Medicine

Pub Date : 2024-12-08 DOI: 10.1016/j.mbm.2024.100111

Sara J. Olsen , Rose E. Leader , Abigail L. Mortimer , Bethany Almeida

Human mesenchymal stem cells (hMSCs) have immense wound healing potential due to their immunomodulatory behavior. To control this behavior and reduce heterogeneity, researchers look to biomaterials, as matrix stiffness and viscoelasticity have been shown to control hMSC immunomodulation. However, the understanding of the effects of these biophysical cues on hMSC immunomodulation remains limited; a broad study investigating the potentially synergistic effects of matrix stiffness and viscoelasticity on hMSC immunomodulation is needed in order to support future work developing biomaterials for hMSC wound healing applications. We developed polyacrylamide (PAAm) gels with varying matrix stiffnesses with or without a viscoelastic element and explored the effects of these on hMSC-matrix interactions and immunomodulatory cytokine expression in both a normal growth media and an immunomodulatory growth media mimetic of a chronic, non-healing wound. Expression of IL-10, VEGF, and PGE₂ were upregulated in immunomodulatory growth media over normal growth media, demonstrating the synergistic effects of biochemical signaling on hMSC immunomodulatory behavior. In addition, the addition of a viscoelastic element had both inhibitory and accentuating effects based on the cytokine and biochemical signaling in the cell culture media. Overall, this study provides a broad perspective on the immunomodulatory behavior of hMSCs due to stiffness and viscoelasticity.

人间充质干细胞（hMSCs）由于其免疫调节行为而具有巨大的伤口愈合潜力。为了控制这种行为并减少异质性，研究人员将目光投向生物材料，因为基质刚度和粘弹性已被证明可以控制hMSC的免疫调节。然而，对这些生物物理线索对造血干细胞免疫调节的影响的理解仍然有限；为了支持未来开发用于hMSC伤口愈合应用的生物材料，需要开展一项广泛的研究，调查基质刚度和粘弹性对hMSC免疫调节的潜在协同作用。我们开发了具有不同基质刚度的聚丙烯酰胺（PAAm）凝胶，有或没有粘弹性元件，并探索了这些凝胶在正常生长介质和模拟慢性不愈合伤口的免疫调节生长介质中对hmsc -基质相互作用和免疫调节细胞因子表达的影响。免疫调节性生长介质中IL-10、VEGF和PGE2的表达较正常生长介质上调，显示生化信号对hMSC免疫调节行为的协同作用。此外，根据细胞培养基中的细胞因子和生化信号，添加粘弹性元件具有抑制和增强作用。总的来说，本研究为hMSCs由于刚度和粘弹性的免疫调节行为提供了广阔的视角。

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引用次数: 0

The first embryo, the origin of cancer and animal phylogeny. V. Cancer stem cells as the unifying biomechanical principle between embryology and oncology 第一个胚胎，癌症的起源和动物系统发育。五、肿瘤干细胞作为胚胎学和肿瘤学之间统一的生物力学原理

Mechanobiology in Medicine

Pub Date : 2024-12-05 DOI: 10.1016/j.mbm.2024.100110

Jaime Cofre

The role of embryology in metazoan evolution is rooted deeply in the history of science. Viewing Neoplasia as an evolutionary engine provides a scientific basis for reexamining the disease cancer. Once the embryo is understood as a benign tumor with a pivotal role in the evolution of all animal forms, there will be an immediate paradigm shift in the search for cancer cure, potentially revealing insights that may be buried within the great developmental transitions of metazoans. This article discusses one of the unifying principles between embryology and oncology, namely cancer stem cells. Some considerations are also provided on the central role of physics and biomechanics in the assembly of the first embryo, which can be regarded as a differentiated benign tumor. Mechanical impregnation of the nucleus of a stem cell, culminating in a totipotent/multipotent cell, was a major event safeguarding the success of embryogenesis throughout evolution. Germ cells in the earliest ctenophore embryos underwent delayed differentiation, subsequent to the mechanical assembly of the embryo. Finally, a discussion is presented on the concept that cancer and embryogenesis (cancer and healthy stem cells) are two sides of the same coin, that is, of the same process. The only difference is that cancer stem cells reveal themselves in inappropriate contexts. Neoplasia is a free force, whereas cancer is a force contained by animal organization.

胚胎学在后生动物进化中的作用深深植根于科学史。视肿瘤为进化引擎为重新审视癌症提供了科学依据。一旦胚胎被理解为一种良性肿瘤，在所有动物形式的进化中起着关键作用，在寻找癌症治疗方面将立即发生范式转变，潜在地揭示可能隐藏在后生动物巨大发育转变中的见解。本文讨论胚胎学与肿瘤学之间的统一原则之一，即肿瘤干细胞。一些考虑也提供了物理和生物力学的核心作用，在组装的第一个胚胎，这可以被视为一个分化的良性肿瘤。干细胞核的机械浸渍，最终形成全能/多能细胞，是整个进化过程中保证胚胎发生成功的一个重要事件。最早的栉水母胚胎中的生殖细胞经历了延迟分化，随后发生了胚胎的机械组装。最后，讨论了癌症和胚胎发生（癌症和健康干细胞）是同一枚硬币的两面，即同一过程的概念。唯一的区别是，癌症干细胞会在不合适的环境中暴露自己。肿瘤是一种自由的力量，而癌症是一种被动物组织所控制的力量。

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引用次数: 0