重组水蛭素和 PAR-1 可调节弥漫大 B 细胞淋巴瘤中巨噬细胞的极化状态

IF 3.5 3区 生物学 Q2 BIOTECHNOLOGY & APPLIED MICROBIOLOGY BMC Biotechnology Pub Date : 2024-08-12 DOI:10.1186/s12896-024-00879-w
Qiang Pei, Zihui Li, Jingjing Zhao, Haixi Zhang, Tao Qin, Juan Zhao
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引用次数: 0

摘要

弥漫大 B 细胞淋巴瘤(DLBCL)是一种恶性肿瘤。虽然一些标准疗法已被确立以提高治愈率,但它们对特定个体仍然无效。因此,寻找更多新的治疗方法意义重大。巨噬细胞极化广泛参与了肿瘤的发展过程。重组水蛭素(rH)会影响巨噬细胞,最近在临床试验中被频繁研究。我们的文章通过收集临床样本验证了 rH 在巨噬细胞极化中的调控作用以及 PAR-1 的作用机制,并随后建立了一个细胞模型,为发现新的治疗方法提供了一个有科学依据的视角。我们评估了临床样本中巨噬细胞极化标志物、细胞因子和 PAR-1 的表达。我们通过与 THP-1 和 OCI-Ly10 细胞共培养建立了细胞模型。我们通过流式细胞术、ELISA 和 RT-qPCR 测定了细胞极化的程度和验证细胞因子的表达,以确认细胞模型的成功。随后,我们加入了不同剂量的 rH,以发现 rH 对细胞极化的作用。我们通过转染 si-PAR-1 和 pcDNA3.1-PAR-1 证实了 PAR-1 在巨噬细胞极化中的作用机制。我们发现在32个DLBCL样本中,M2巨噬细胞标志物(CD163 + CMAF+)和PAR-1的表达较高。在诱导单核细胞分化为 M0 巨噬细胞并与 OCI-Ly10 淋巴瘤细胞共培养后,我们发现细胞模型中这些表达的趋势与临床样本一致。随后,我们发现 rH 可促进 M1 巨噬细胞的极化,但会抑制 M2 巨噬细胞的极化。我们还发现,PAR-1 可调节巨噬细胞的极化,抑制细胞的增殖、迁移、侵袭和血管生成能力。
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Recombinant hirudin and PAR-1 regulate macrophage polarisation status in diffuse large B-cell lymphoma
Diffuse large B-cell lymphoma (DLBCL) is a malignant tumour. Although some standard therapies have been established to improve the cure rate, they remain ineffective for specific individuals. Therefore, it is meaningful to find more novel therapeutic approaches. Macrophage polarisation is extensively involved in the process of tumour development. Recombinant hirudin (rH) affects macrophages and has been researched frequently in clinical trials lately. Our article validated the regulatory role of rH in macrophage polarisation and the mechanism of PAR-1 by collecting clinical samples and subsequently establishing a cellular model to provide a scientifically supported perspective for discovering new therapeutic approaches. We assessed the expression of macrophage polarisation markers, cytokines and PAR-1 in clinical samples. We established a cell model by co-culture with THP-1 and OCI-Ly10 cell. We determined the degree of cell polarisation and expression of validation cytokines by flow cytometry, ELISA, and RT-qPCR to confirm the success of the cell model. Subsequently, different doses of rH were added to discover the function of rH on cell polarisation. We confirmed the mechanism of PAR-1 in macrophage polarisation by transfecting si-PAR-1 and pcDNA3.1-PAR-1. We found higher expression of M2 macrophage markers (CD163 + CMAF+) and PAR-1 in 32 DLBCL samples. After inducing monocyte differentiation into M0 macrophages and co-culturing with OCI-Ly10 lymphoma cells, we found a trend of these expressions in the cell model consistent with the clinical samples. Subsequently, we discovered that rH promotes the polarisation of M1 macrophages but inhibits the polarisation of M2 macrophages. We also found that PAR-1 regulates macrophage polarisation, inhibiting cell proliferation, migration, invasion and angiogenic capacity. rH inhibits macrophage polarisation towards the M2 type and PAR-1 regulates polarisation, proliferation, migration, invasion, and angiogenesis of DLBCL-associated macrophages.
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来源期刊
BMC Biotechnology
BMC Biotechnology 工程技术-生物工程与应用微生物
CiteScore
6.60
自引率
0.00%
发文量
34
审稿时长
2 months
期刊介绍: BMC Biotechnology is an open access, peer-reviewed journal that considers articles on the manipulation of biological macromolecules or organisms for use in experimental procedures, cellular and tissue engineering or in the pharmaceutical, agricultural biotechnology and allied industries.
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