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

• Published in: Frontiers in cell and developmental biology 2021-04, Vol.9, p.645005-645005
• Main Authors: Yong, Jiawen, von Bremen, Julia, Ruiz-Heiland, Gisela, Ruf, Sabine
• Format: Article
• Language: English
• Subjects: adiponectin; Cell and Developmental Biology; cementoblast; compression; MAPK pathway; β-catenin
• ISSN: 2296-634X; 2296-634X
• DOI: 10.3389/fcell.2021.645005

We aimed to investigate the molecular effect that adiponectin exerts on cementoblasts especially in the presence of compressive forces. OCCM-30 cells (M. Somerman, NIH, NIDCR, United States) were used. Real-time reverse transcriptase-polymerase chain reaction (RT-PCR) and western blots were employed to verify if the mRNA and protein levels of adiponectin receptors (AdipoRs), mitogen-activated protein kinase (MAPK), and β-catenin signaling were influenced by compressive forces or adiponectin. Moreover, siRNAs targeting α, , , , and as well as pharmacological MAPK inhibition were performed. We found that compressive forces increase the expression of . Adiponectin and compression up-regulate α, , , and as well as β- gene expression. Western blots showed that co-stimuli activate the MAPK and β-catenin signaling pathways. MAPK inhibition alters the compression-induced β-catenin activation and the siRNAs targeting , α, and , showing the interaction of single MAPK molecules and β-catenin signaling in response to compression or adiponectin. Silencing by a dominantly negative version of α and attenuates adiponectin-induced TCF/LEF reporter activation. Together, we found that light compressive forces activate β-catenin and MAPK signaling pathways. Adiponectin regulates β-catenin signaling principally by inactivating the GSK-3β kinase activity. β-Catenin expression was partially inhibited by MAPK blockade, indicating that MAPK plays a crucial role regulating β-catenin during cementogenesis. Moreover, adiponectin modulates GSK-3β and β-catenin mostly through AdipoR1. P38α is a key connector between β-catenin, TCF/LEF transcription, and MAPK signaling pathway.