Sun-Kyung Lee and Jong-Hyuk Chung contributed equally to this work.
Sodium hydrogen sulfide inhibits nicotine and lipopolysaccharide-induced osteoclastic differentiation and reversed osteoblastic differentiation in human periodontal ligament cells†
Article first published online: 14 MAR 2013
Copyright © 2012 Wiley Periodicals, Inc.
Journal of Cellular Biochemistry
Volume 114, Issue 5, pages 1183–1193, May 2013
How to Cite
Lee, S.-K., Chung, J.-H., Choi, S.-C., Auh, Q.-S., Lee, Y.-M., Lee, S.-I. and Kim, E.-C. (2013), Sodium hydrogen sulfide inhibits nicotine and lipopolysaccharide-induced osteoclastic differentiation and reversed osteoblastic differentiation in human periodontal ligament cells. J. Cell. Biochem., 114: 1183–1193. doi: 10.1002/jcb.24461
- Issue published online: 14 MAR 2013
- Article first published online: 14 MAR 2013
- Accepted manuscript online: 28 NOV 2012 08:27AM EST
- Manuscript Accepted: 7 NOV 2012
- Manuscript Received: 23 MAY 2012
- Kyung Hee University. Grant Number: KHU-20111734
- HYDROGEN SULFIDE;
- PERIODONTAL LIGAMENT CELLS
Although previous studies have demonstrated that hydrogen sulfide (H2S) stimulated or inhibited osteoclastic differentiation, little is known about the effects of H2S on the differentiation of osteoblasts and osteoclasts. To determine the possible bioactivities of H2S on bone metabolism, we investigated the in vitro effects of H2S on cytotoxicity, osteoblastic, and osteoclastic differentiation as well as the underlying mechanism in lipopolysaccharide (LPS) and nicotine-stimulated human periodontal ligament cells (hPDLCs). The H2S donor, NaHS, protected hPDLCs from nicotine and LPS-induced cytotoxicity and recovered nicotine- and LPS-downregulated osteoblastic differentiation, such as alkaline phosphatase (ALP) activity, mRNA expression of osteoblasts, including ALP, osteopontin (OPN), and osteocalcin (OCN), and mineralized nodule formation. Concomitantly, NaHS inhibited the differentiation of tartrate-resistant acid phosphatase (TRAP)-positive osteoclasts in mouse bone marrow cells and blocked nicotine- and LPS-induced osteoclastogenesis regulatory molecules, such as RANKL, OPG, M-CSF, MMP-9, TRAP, and cathepsin K mRNA. NaHS blocked nicotine and LPS-induced activation of p38, ERK, MKP-1, PI3K, PKC, and PKC isoenzymes, and NF-κB. The effects of H2S on nicotine- and LPS-induced osteoblastic and osteoclastic differentiation were remarkably reversed by MKP-1 enzyme inhibitor (vanadate) and expression inhibitor (triptolide). Taken together, we report for the first time that H2S inhibited cytotoxicity and osteoclastic differentiation and recovered osteoblastic differentiation in a nicotine- and periodontopathogen-stimulated hPDLCs model, which has potential therapeutic value for treatment of periodontal and inflammatory bone diseases. J. Cell. Biochem. 114: 1183–1193, 2013. © 2012 Wiley Periodicals, Inc.