4.6 Article

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

Journal

Publisher

ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbrc.2021.08.086

Keywords

Osteogenic differentiation; Osteomyelitis; Staphylococcus A protein; NONHSAT009968; Long non-coding RNA; Human bone marrow mesenchymal stem cells

Funding

  1. National Natural Science Foundation of China [81772367, 82072392]
  2. Applied Basic Research Joint Project of Yunnan Provincial Science and Technology Department and Kunming Medical University

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The study revealed that NONHSAT009968 inhibited the osteogenic differentiation of hBMMSCs under infection through the Wnt3a pathway, which may have affected the occurrence and development of osteomyelitis.
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. (c) 2021 The Authors. Published by Elsevier Inc. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

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