TITLE:
Influence of Adiponectin and Leptin on the Kinetics of Human Pulp Cells
AUTHORS:
Isao Tamura, Katsura Ueda, Yoshifumi Matsuda, Aiko Kamada, Yoshihiro Yoshikawa, Eisuke Domae, Takashi Ikeo, Shunji Kumabe
KEYWORDS:
Dental Pulp Cells, Adiponectin, Leptin, Bone Morphogenetic Protein-2, Dentin Sialoprotein, Osteopontin, ECM Formation
JOURNAL NAME:
Open Journal of Stomatology,
Vol.10 No.12,
December
17,
2020
ABSTRACT: Adipocytokines, such as adiponectin and leptin, are expressed by adipocytes and are known as anti-metabolic syndrome factors. They are also thought to mediate calcification in mineralized tissue. We investigated the effects of adiponectin and leptin on the kinetics of human pulp cells using ELISA and western blot. After gaining informed consent, we obtained human pulp cells from three patients. After cultivation in Dulbecco’s Modified Eagle Medium (DMEM) without serum, cells from the 4th to 6th passages were incubated with various concentrations of adiponectin (1, 10, or 100 ng/mL) in DMEM or leptin (0.1, 1, or 10 ng/mL) in DMEM for 24 h. We confirmed that human pulp cells expressed adiponectin receptor 1 and leptin receptor. Although the proliferation index of these cells as measured by 5-bromo-2'-deoxyuridine (BrdU) incorporation increased in the presence of adiponectin in a dose-dependent manner, pulp cells stimulated with leptin showed no significant changes in BrdU incorporation. Alkaline phosphatase activity showed no significant changes after stimulation with either adipocytokine. Adiponectin induced expression of BMP-2 and osteopontin more strongly than did leptin. In particular, expression of BMP-2 increased in the presence of adiponectin in a dose-dependent manner. In contrast, the expression of dentin sialoprotein increased after stimulation with leptin. The expression of Runx2 was not observed from the cultured pulp cells stimulated with both molecules. These results indicate that adiponectin and leptin contribute to growth and differentiation of human pulp cells and may consequently affect the formation of secondary dentin or reparative dentin in the dentin-pulp complex.