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敲低人骨髓间充质干细胞中的核心蛋白聚糖可抑制蛋白聚糖层形成,并在二氧化钛表面建立促炎环境。

Knockdown of decorin in human bone marrow mesenchymal stem cells suppresses proteoglycan layer formation and establishes a pro-inflammatory environment on titanium oxide surfaces.

作者信息

Kamio Hisanobu, Okabe Kazuto, Honda Masaki, Kuroda Kensuke, Tsuchiya Shuhei

机构信息

Department of Dental Anesthesiology, Division of Oral and Maxillofacial Surgery and Oral Medicine, Hiroshima University Hospital, Hiroshima city, Hiroshima, Japan.

Department of Oral and Maxillofacial Surgery, Nagoya City University Graduate School of Medical Sciences, Nagoya, Aichi, Japan.

出版信息

J Mater Sci Mater Med. 2025 Jan 7;36(1):5. doi: 10.1007/s10856-024-06849-0.

Abstract

Osseointegration is essential for successful implant treatment. However, the underlying molecular mechanisms remain unclear. In this study, we focused on decorin (DCN), which was hypothesized to be present in the proteoglycan (PG) layer at the interface between bone and the titanium oxide (TiOx) surface. We utilized DCN RNA interference in human bone marrow mesenchymal stem cells (hBMSCs) to investigate its effects on PG layer formation, proliferation, initial adhesion, cell extension, osteogenic capacity, fibrotic markers, and immunotolerance to TiOx in vitro. After 14 days of cultivation, we observed no PG layer was detected, and the osteogenic capacity was suppressed in DCN-depleted hBMSCs. Furthermore, the conditioned medium upregulated the expression of M1 macrophage markers in human macrophages. These results suggest that endogenous DCN plays a crucial role in PG layer formation and that the PG layer alters inflammation around Ti materials.

摘要

骨结合对于成功的种植治疗至关重要。然而,其潜在的分子机制仍不清楚。在本研究中,我们聚焦于核心蛋白聚糖(DCN),据推测它存在于骨与二氧化钛(TiOx)表面界面处的蛋白聚糖(PG)层中。我们利用人骨髓间充质干细胞(hBMSCs)中的DCN RNA干扰来研究其对PG层形成、增殖、初始黏附、细胞伸展、成骨能力、纤维化标志物以及体外对TiOx的免疫耐受性的影响。培养14天后,我们观察到在DCN缺失的hBMSCs中未检测到PG层,并且成骨能力受到抑制。此外,条件培养基上调了人巨噬细胞中M1巨噬细胞标志物的表达。这些结果表明内源性DCN在PG层形成中起关键作用,并且PG层改变了钛材料周围的炎症反应。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/114a/11706895/1f5771bb7e7d/10856_2024_6849_Fig1_HTML.jpg

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