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长非编码 RNA NONHSAT009968 通过 Wnt3a 抑制 SA 诱导的炎症中的 hBMMSCs 成骨分化。

LncRNA NONHSAT009968 inhibits the osteogenic differentiation of hBMMSCs in SA-induced inflammation via Wnt3a.

机构信息

Department of Orthopaedic and Traumatic Surgery, The Second People's Hospital of Yunnan Province, Kunming, China; Department of Orthopaedic and Traumatic Surgery, The Affiliated Hospital of Yunnan University, Kunming, China.

Department of Orthopaedic Surgery, 920th Hospital of Joint Logistics Support Force, Kunming, China.

出版信息

Biochem Biophys Res Commun. 2021 Nov 5;577:24-31. doi: 10.1016/j.bbrc.2021.08.086. Epub 2021 Sep 2.

Abstract

Osteomyelitis is one of the most challenging diseases in the field of orthopedics for its complex pathogenesis and unsatisfactory treatment. The mechanism underlying its occurrence and development is still unclear. In our previous study, we found that long non-coding RNA (lncRNA) NONHSAT009968 inhibited the ability of osteogenic differentiation in staphylococcal protein A (SPA)-treated human bone marrow mesenchymal stem cells (hBMMSCs), but the underlying mechanism remains unclear. The current study was aimed at elucidating the possible mechanism of NONHSAT009968 in regulating osteogenic differentiation and bone defect repairability of hBMMSCs under infection. It was revealed that Wnt3a played a key role in promoting osteogenic differentiation of hBMMSCs treated with SPA in vitro. In addition, NONHSAT009968 inhibited osteogenic differentiation of hBMMSCs treated with SPA via Wnt3a, both in vivo and in vitro. In sum, the results suggested that lncNONHSAT009968 inhibited osteogenic differentiation of hBMMSCs in SA-induced inflammation through Wnt3a, which may have affected the occurrence and development of osteomyelitis. This study might provide novel insights regarding osteomyelitis and infectious bone defects.

摘要

骨髓炎是骨科领域最具挑战性的疾病之一,其发病机制复杂,治疗效果不理想。其发生发展的机制尚不清楚。在我们之前的研究中,我们发现长链非编码 RNA (lncRNA) NONHSAT009968 抑制了金黄色葡萄球菌蛋白 A (SPA)处理的人骨髓间充质干细胞 (hBMMSCs) 的成骨分化能力,但潜在机制尚不清楚。本研究旨在阐明 NONHSAT009968 在感染条件下调节 hBMMSCs 成骨分化和骨缺损修复能力的可能机制。结果表明,Wnt3a 在体外 SPA 处理的 hBMMSCs 成骨分化中起关键作用。此外,NONHSAT009968 通过 Wnt3a 抑制 SPA 处理的 hBMMSCs 的成骨分化,无论是在体内还是体外。总之,这些结果表明,lncNONHSAT009968 通过 Wnt3a 抑制 SA 诱导的炎症中 hBMMSCs 的成骨分化,这可能影响了骨髓炎的发生和发展。本研究可能为骨髓炎和感染性骨缺损提供新的见解。

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