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口腔细胞裂解物可减少小鼠骨髓培养物中的破骨细胞生成。

Oral cell lysates reduce osteoclastogenesis in murine bone marrow cultures.

作者信息

Panahipour Layla, Abbasabadi Azarakhsh Oladzad, Shao Feng, Gruber Reinhard

机构信息

Department of Oral Biology, University Clinic of Dentistry, Medical University of Vienna, Sensengasse 2a, 1090 Vienna, Austria.

Department of Periodontology, School of Dental Medicine, University of Bern, 3010 Bern, Switzerland.

出版信息

Cytotechnology. 2025 Feb;77(1):39. doi: 10.1007/s10616-024-00688-1. Epub 2025 Jan 8.

Abstract

Mechanical and thermal cell damage can occur due to invasive procedures related to drilling, the insertion of dental implants, and periodontal treatments. Necrotic cells release the content of their cytoplasm and membrane fragments, thereby signaling the need for repair, which includes bone resorption by osteoclasts and inflammation. Here we screened lysates from human gingival fibroblasts, HSC2 and TR146 oral squamous carcinoma cell lines, as well as murine IDG-SW3 osteocytic and RAW264.7 macrophage cell lines for their potential to modulate in vitro osteoclastogenesis in murine bone marrow cultures. We also tested the impact of necrotic lysates on modulating the expression of inflammatory cues in murine ST2 bone marrow stromal cells. We report here that independent of human or murine origin, all cell lysates significantly reduced in vitro osteoclastogenesis in bone marrow cultures, as indicated by the expression of the osteoclast marker genes cathepsin K and tartrate-resistant acid phosphatase and the respective histochemical staining in multinucleated cells. We also found that lysates from HSC2 and TR146 cells significantly pushed the expression of CCL2, CCL5, CXCL1, IL1, and IL6 in ST2 cells. These findings suggest that oral cell lysates reduce in vitro osteoclastogenesis, but only damaged oral squamous carcinoma cells can force murine stromal cells to produce an inflammatory environment.

摘要

与钻孔、牙种植体植入和牙周治疗相关的侵入性操作可能会导致细胞受到机械和热损伤。坏死细胞会释放其细胞质内容物和膜碎片,从而发出修复信号,这包括破骨细胞介导的骨吸收和炎症反应。在此,我们筛选了来自人牙龈成纤维细胞、HSC2和TR146口腔鳞状癌细胞系,以及小鼠IDG-SW3骨细胞和RAW264.7巨噬细胞系的裂解物,以评估它们在体外调节小鼠骨髓培养物中破骨细胞生成的潜力。我们还测试了坏死裂解物对调节小鼠ST2骨髓基质细胞中炎症信号表达的影响。我们在此报告,无论来源是人还是小鼠,所有细胞裂解物均显著降低了骨髓培养物中的体外破骨细胞生成,这通过破骨细胞标记基因组织蛋白酶K和抗酒石酸酸性磷酸酶的表达以及多核细胞中的相应组织化学染色得以体现。我们还发现,HSC2和TR146细胞的裂解物显著促进了ST2细胞中CCL2、CCL5、CXCL1、IL1和IL6的表达。这些发现表明,口腔细胞裂解物可降低体外破骨细胞生成,但只有受损的口腔鳞状癌细胞才能促使小鼠基质细胞产生炎症环境。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a4e3/11707159/014e3315d3c0/10616_2024_688_Fig1_HTML.jpg

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