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培养的原代牙龈细胞和牙周膜细胞对血管紧张素II和白细胞介素1β刺激的反应。

Response of cultured primary gingival and periodontal ligament cells to angiotensin II and IL1β challenges.

作者信息

Garbieri Thais Francini, Dionísio Thiago José, Colombini-Ishikiriama Bella Luna, Silva Rafaela Alves da, Lara Vanessa Soares, Oliveira Sandra Helena Penha, Fernandes Maria Helena, Greene Andrew Seth, Santos Carlos Ferreira

机构信息

Universidade de São Paulo - USP, Bauru School of Dentistry, Department of Biological Sciences, Bauru, SP, Brazil.

Universidade de São Paulo - USP, Bauru School of Dentistry, Department of Surgery, Stomatology, Pathology and Radiology, Bauru, SP, Brazil.

出版信息

Braz Oral Res. 2025 Sep 8;39:e083. doi: 10.1590/1807-3107bor-2025.vol39.083. eCollection 2025.

Abstract

Angiotensin II (Ang II) releases inflammatory mediators from several cell types. The objective of this study was to investigate the potential of Ang II to induce mRNA expression of inflammatory mediators in primary cultured fibroblast-like cells isolated from gingival and periodontal ligament tissues. A synergistic effect of co-treatment with Ang II and Interleukin-1β (IL1β) on the mRNA expression of inflammatory mediators was explored. Immunophenotyping of STRO-1, Ang II type 1 receptor (AT1R), and Ang II type 2 receptor (AT2R) was performed using flow cytometry. Cell cultures were challenged with Ang II (1 µM) for 3, 6, and 24 h with or without co-treatment with IL1β (0.1 ng/mL) for 24 h. mRNA expression of inflammatory mediators was determined using qPCR. We present, for the first time, precise quantification of AT1R and AT2R in human gingival and periodontal fibroblast-like cell types; the percentage of positive immunostaining compared to the total cell population varied from 3.35% to 5.29% for AT1R and 2.97% to 4.57% for AT2R. Ang II slightly upregulated IL6 and CCL2/MCP1 mRNA expression in gingival cells and IL8 and PTGS2/COX2 in periodontal ligament cells. IL1β upregulated IL8, IL6, CCL2/MCP1, PTGS2/COX2, and IL1β mRNA in both cell types. Co-treatment with Ang II and IL1β did not show a synergistic effect. Ang II showed a low potential to induce mRNA of inflammatory mediators, most likely owing to the low percentage of Ang II receptors in such cells and no synergistic effect with the co-treatment with IL1β.

摘要

血管紧张素 II(Ang II)可从多种细胞类型中释放炎症介质。本研究的目的是调查 Ang II 在从牙龈和牙周韧带组织分离的原代培养成纤维样细胞中诱导炎症介质 mRNA 表达的潜力。探讨了 Ang II 与白细胞介素 -1β(IL1β)联合处理对炎症介质 mRNA 表达的协同作用。使用流式细胞术对 STRO-1、血管紧张素 II 1 型受体(AT1R)和血管紧张素 II 2 型受体(AT2R)进行免疫表型分析。细胞培养物用 Ang II(1 μM)处理 3、6 和 24 小时,有或没有与 IL1β(0.1 ng/mL)联合处理 24 小时。使用 qPCR 测定炎症介质的 mRNA 表达。我们首次精确量化了人牙龈和牙周成纤维样细胞类型中 AT1R 和 AT2R 的表达;与总细胞群体相比,AT1R 的阳性免疫染色百分比在 3.35% 至 5.29% 之间,AT2R 的阳性免疫染色百分比在 2.97% 至 4.57% 之间。Ang II 轻微上调牙龈细胞中 IL6 和 CCL2/MCP1 的 mRNA 表达,以及牙周韧带细胞中 IL8 和 PTGS2/COX 的 mRNA 表达。IL1β 上调两种细胞类型中 IL8、IL6、CCL2/MCP1、PTGS2/COX2 和 IL1β 的 mRNA 表达。Ang II 与 IL1β 联合处理未显示协同作用。Ang II 诱导炎症介质 mRNA 的潜力较低,这很可能是由于此类细胞中 Ang II 受体的百分比低,并且与 IL1β 联合处理没有协同作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/61a7/12419197/b868dfd44d98/1807-3107-bor-39-e083-gf01.jpg

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