Adiponectin inhibits lipoplysaccharide-induced inflammation and promotes osteogenesis in hPDLCs
Authors: Yuan Guo
Huan-Huan Wu
Zhi-Hui Tang
Yin-Fei Pu
Journal: Bioscience Reports (2021)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: adiponectin; human periodontal ligament cells; inflammation; lipopolysaccharide; osteogenic differentiation.
Affiliations: Second Dental Center, School and Hospital of Stomatology, Peking University, Beijing 100081, People’s Republic of China, National Engineering Laboratory for Digital and Material Technology of Stomatology, School and Hospital of Stomatology, Peking University, Beijing 100081, People’s Republic of China

Abstract:  Periodontal diseases are infections of the structures that surround and support the teeth; they are characterized by local inflammation and alveolar bone loss. Most treatments focus on only one aspect, inhibiting inflammation, or promoting osteoblasts. We set out to develop a new method that would intervene in the two aspects simultaneously. Adiponectin (APN), secreted by adipocytes, inhibits the inflammatory response and promotes osteogenesis. However, its role in human periodontal ligament cells (hPDLCs) is unclear. Therefore, we aim to investigate whether APN could suppress lipopolysaccharide (LPS)-induced inflammation and promote osteogenesis in hPDLCs. In the present study, we stimulated hPDLCs with LPS in the presence or absence of APN. Real-time PCR and Western blotting results demonstrated that APN partially inhibited the activation of the classical nuclear factor κ-B (NF-κB) pathway. These results were confirmed by a change of expressions of NF-κB downstream inflammatory genes, such as decreased cyclooxygenase (COX)-2 and tumor necrosis factor α (TNF-α), along with increased interleukin (IL)-10. As for the role of APN in osteogenesis, Alizarin Red S staining showed that APN treatment induced more calcium deposition nodules than controls. We also found that APN enhanced the expression of osteoblast-related genes (osteopontin (OPN), collagen 1, osteocalcin, alkaline phosphatase, runt-related transcription factor 2 (RUNX2), and bone morphogenetic protein 2) in hPDLCs via the APPL1 (the adaptor protein containing PH domain, PTB domain, and leucine zipper motif 1)/p38 signal transduction pathway. Therefore, APN inhibits LPS-induced inflammation and promotes osteogenesis in hPDLCs and may have potential therapeutic value in treating periodontitis by inhibiting the inflammatory lesions and contributing to bone tissue regeneration. 

Retracted: No

PubPeer comments:
 Images in 5B and 7B appear to overlap. Perhaps in one case it is intentional. Could the authors comment? *** ![file] ![file] *** ![file] *** ![file] , 
 Corrected [2 July 2021] . ------------------------------------- This Correction follows an Expression of Concern relating to this article previously published by Portland Press. The Authors of the original article u201cAdiponectin inhibits lipoplysaccharide-induced inflammation and promotes osteogenesis in hPDLCsu201d (Biosci Rep (2021) 41(3), https: doi.org 10.1042 BSR20192668) would like to correct Figure 5B and 7B, as a duplication of these images had occurred due to an error in their figure making process. The Authors have repeated the experiment and present the correct Figure 7B here. The Authors confirm that this Correction does not change the conclusions of their study. ![file] ,