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人羊膜间充质干细胞在糖脂毒性环境下促进人骨髓间充质干细胞成骨。

Human amnion-derived mesenchymal stem cells promote osteogenesis of human bone marrow mesenchymal stem cells against glucolipotoxicity.

机构信息

Jiangsu Key Laboratory of Oral Diseases Nanjing Medical University China.

Department of Dental Implant Affiliated Hospital of Stomatology Nanjing Medical University China.

出版信息

FEBS Open Bio. 2018 Nov 26;9(1):74-81. doi: 10.1002/2211-5463.12547. eCollection 2019 Jan.

DOI:10.1002/2211-5463.12547
PMID:30652075
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6325622/
Abstract

Epidemiological evidence suggests that diabetes mellitus (DM) is an important factor in promoting periodontitis. It not only affects the attachment of connective tissue but also causes loss of alveolar bone. Hence, there is an urgent need to find an effective treatment for DM-induced bone deficiency. This study aimed to investigate the effects of human amniotic mesenchymal stem cells (HAMSCs) on the proliferation and osteogenic differentiation of DM-induced human bone marrow mesenchymal stem cells (HBMSCs). High glucose and palmitic acid (GP) were used to mimic DM-induced glucolipotoxicity. The proliferation levels were measured using flow cytometry. Alkaline phosphatase activity substrate assays, Alizarin red S staining, and western blotting were used to investigate osteogenic differentiation. Oxidative stress was measured by assaying the levels of reactive oxygen species. This study found that glucolipotoxicity caused by GP remarkably inhibited cell proliferation and osteogenesis, and upregulated the oxidative stress level in HBMSCs. However, HAMSCs attenuated HBMSC dysfunction through antioxidant activity by influencing p38 mitogen-activated protein kinase and vascular endothelial growth factor secretion. In conclusion, our findings indicate that HAMSCs might be suitable for treating DM-mediated bone deficiency.

摘要

流行病学证据表明,糖尿病(DM)是促进牙周炎的一个重要因素。它不仅影响结缔组织的附着,还导致牙槽骨丧失。因此,迫切需要找到一种有效的治疗方法来治疗 DM 引起的骨缺损。本研究旨在探讨人羊膜间充质干细胞(HAMSCs)对 DM 诱导的人骨髓间充质干细胞(HBMSCs)增殖和成骨分化的影响。高葡萄糖和棕榈酸(GP)用于模拟 DM 诱导的糖脂毒性。通过流式细胞术测量增殖水平。碱性磷酸酶活性底物测定、茜素红 S 染色和 Western blot 用于研究成骨分化。通过测定活性氧水平来测量氧化应激。本研究发现,GP 引起的糖脂毒性显著抑制 HBMSCs 的增殖和成骨,并上调 HBMSCs 的氧化应激水平。然而,HAMSCs 通过影响 p38 丝裂原活化蛋白激酶和血管内皮生长因子的分泌,通过抗氧化活性来减轻 HBMSC 功能障碍。总之,我们的研究结果表明,HAMSCs 可能适合治疗 DM 介导的骨缺损。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eeda/6325622/c5a1b2243c07/FEB4-9-74-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eeda/6325622/934e54c7853e/FEB4-9-74-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eeda/6325622/f612dfd7d1c3/FEB4-9-74-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eeda/6325622/88253a837db2/FEB4-9-74-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eeda/6325622/c5a1b2243c07/FEB4-9-74-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eeda/6325622/934e54c7853e/FEB4-9-74-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eeda/6325622/f612dfd7d1c3/FEB4-9-74-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eeda/6325622/88253a837db2/FEB4-9-74-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eeda/6325622/c5a1b2243c07/FEB4-9-74-g004.jpg

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本文引用的文献

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