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胶原处理时原发性骨细胞与骨髓巨噬细胞间的对话促进破骨细胞生成。

Cross-talk between primary osteocytes and bone marrow macrophages for osteoclastogenesis upon collagen treatment.

机构信息

Department of Marine Bio-Pharmacology, College of Food Science and Technology, Shanghai Ocean University, Shanghai, 201306, China.

Bone and Cartilage Research Unit, Arthropôle Liège, University of Liège, CHU Sart-Tilman, Liège, 4000, Belgium.

出版信息

Sci Rep. 2018 Mar 28;8(1):5318. doi: 10.1038/s41598-018-23532-x.

Abstract

Homeostasis of osteoclast formation from bone marrow macrophages (BMM) is regulated by paracrine signals of the neighbourhood bone cells particularly mesenchymal stem cells (MSC), osteoblasts and osteocytes (OC). Besides paracrine cues, collagen and glycosaminoglycan are involved in controlling bone homeostasis. Towards this approach, different molecular weight collagens were reacted with MSC, OC and BMM to understand the bone homeostasis activity of collagen. The up-regulating effect of collagens on osteogenic cell growth was confirmed by the presence of mineralized nodules in the osteoblastogenic lineage cells and increased osteogenic stimulatory gene expression. The decreased BMM-derived TRAP+ osteoclasts number and osteoclastogenic regulatory gene expression of OC could demonstrate the exploitive osteoclastogenic activity of collagens. Osteoclastogenesis from BMM was triggered by paracrine cues of OC in some extend, but it was down-regulated by collagen. Overall, the effect of collagen on osteoclastogenesis and osteoblastogenesis may depend on the molecular weight of collagens, and collagen suppresses osteoclastogenesis, at least in part by downregulating the secretion of cytokines in OC.

摘要

破骨细胞形成的骨稳态由骨髓巨噬细胞(BMM)的旁分泌信号调节,特别是间充质干细胞(MSC)、成骨细胞和骨细胞(OC)。除了旁分泌线索外,胶原蛋白和糖胺聚糖也参与控制骨骼稳态。为此,我们将不同分子量的胶原蛋白与 MSC、OC 和 BMM 反应,以了解胶原蛋白对骨骼稳态的活性。胶原蛋白对成骨细胞生长的上调作用通过矿化结节在成骨细胞系细胞中的存在和增加的成骨刺激基因表达得到证实。OC 中破骨细胞生成的 BMM 衍生的 TRAP+数量减少和破骨细胞生成调节基因表达可以证明胶原蛋白具有破骨细胞生成活性。BMM 中的破骨细胞发生在一定程度上受 OC 的旁分泌信号触发,但被胶原蛋白下调。总的来说,胶原蛋白对破骨细胞生成和成骨细胞生成的影响可能取决于胶原蛋白的分子量,并且胶原蛋白至少部分通过下调 OC 中细胞因子的分泌来抑制破骨细胞生成。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7b19/5871752/c3d100f96a32/41598_2018_23532_Fig1_HTML.jpg

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