Adiponectin Interacts In-Vitro With Cementoblasts Influencing Cell Migration, Proliferation and Cementogenesis Partly Through the MAPK Signaling Pathway

Abstract

Current clinical evidences suggest that circulating Adipokines such as Adiponectin can influence the ratio of orthodontic tooth movement. We aimed to investigate the effect that Adiponectin has on cementoblasts (OCCM-30) and on the intracellular signaling molecules of Mitogen-activated protein kinase (MAPK). We demonstrated that OCCM-30 cells express AdipoR1 and AdipoR2. Alizarin Red S staining revealed that Adiponectin increases mineralized nodule formation and quantitative AP activity in a dose-dependent manner. Adiponectin up-regulates the mRNA levels of AP, BSP, OCN, OPG, Runx-2 as well as F-Spondin. Adiponectin also increases the migration and proliferation of OCCM-30 cells. Moreover, Adiponectin induces a transient activation of JNK, P38, ERK1/2 and promotes the phosphorylation of STAT1 and STAT3. The activation of Adiponectin-mediated migration and proliferation was attenuated after pharmacological inhibition of P38, ERK1/2 and JNK in different degrees, whereas mineralization was facilitated by MAPK inhibition in varying degrees. Based on our results, Adiponectin favorably affect OCCM-30 cell migration, proliferation as well as cementogenesis. One of the underlying mechanisms is the activation of MAPK signaling pathway.

Adiponectin as Well as Compressive Forces Regulate in vitro β-Catenin Expression on Cementoblasts via Mitogen-Activated Protein Kinase Signaling Activation

“…This indicates that adiponectin additionally triggers the MAP kinase pathway. In accordance with our previous data (2020), adiponectin strongly induced the expression of phosphorylated P38, ERK1/2, and JNK on cementoblasts ( Yong et al, 2020 ).…”

“…This indicates that adiponectin additionally triggers the MAP kinase pathway. In accordance with our previous data ( 2020), adiponectin strongly induced the expression of phosphorylated P38, ERK1/2, and JNK on cementoblasts (Yong et al, 2020). The cooperative interaction between the β-catenin and MAPK signaling pathways has been reported in several studies (Bikkavilli et al, 2008;Thornton et al, 2008;Bikkavilli and Malbon, 2009;Osaki and Gama, 2013).…”

“…Adiponectin, a secreted protein produced mainly by adipocytes ( Scherer et al, 1995 ), binds to its two receptors (AdipoR1 and AdipoR2) ( Yamauchi et al, 2003 ). Adiponectin and its two receptors were reported to be expressed in primary human osteoblasts ( Lin et al, 2014 ) and cementoblasts ( Yong et al, 2020 ), which act as an important signaling link between fat and body weight to bone density ( Berner et al, 2004 ). Unlike other adipokines such as leptin, the concentration of circulating adiponectin in obese human individuals is significantly lower than in non-obese ( Naot et al, 2017 ).…”

“…Unlike other adipokines such as leptin, the concentration of circulating adiponectin in obese human individuals is significantly lower than in non-obese ( Naot et al, 2017 ). Recently, we elucidated the expression of adiponectin receptors on OCCM-30 cells and revealed that adiponectin has a pro-cementogenesis effect on cementoblasts partly through the MAPK signaling pathway ( Yong et al, 2020 ). However, some research reveal that adiponectin has emerged as a key mediator regulating the anti-inflammatory and anti-apoptotic effects of biological activities ( Tilg and Wolf, 2005 ; Sun and Chen, 2010 ).…”

Hypoxia‐inducible factor 1‐alpha acts as a bridge factor for crosstalk between ERK1/2 and caspases in hypoxia‐induced apoptosis of cementoblasts

“…7 Obese patients have an impaired cementum metabolism, due in part to their altered levels of circulating adipokines. 13,14 Adipokines, produced mainly by adipocytes, which influence apoptosis and inflammatory responses of cementoblasts during OTM in obese individuals. 15 Thus, it is of vital importance to investigate the influence of adipokines on the apoptosis of cementoblasts under the experimental hypoxic setup.…”