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Technetium-99 conjugated with methylene diphosphonate inhibits receptor activator of nuclear factor-κB ligand-induced osteoclastogenesis.
Clin Exp Pharmacol Physiol. 2012 Oct; 39(10):886-93.CE

Abstract

1. In the present study, we investigated the effects of technetium-99 conjugated with methylene diphosphonate ((99)Tc-MDP), an agent used in radionuclide therapy, on receptor activator of nuclear factor-κB ligand (RANKL)-induced osteoclastogenesis and explored the underlying mechanisms. 2. The murine macrophage cell line RAW264.7 and bone marrow-derived-macrophages from C57BL/6 mice (BMM) were used as models for osteoclastogenesis in vitro. The expression of some key factors in RANKL (50 ng/mL)-induced osteoclastogenesis in RAW264.7 cells was investigated by flow cytometry and real-time reverse transcription-polymerase chain reaction (RT-PCR). To detect multinucleated osteoclast formation, RAW264.7 cells were induced with RANKL for 4 days, whereas BMM were induced by 50 ng/mL RANKL and 20 ng/mL macrophage colony-stimulating factor for 7 days, before being stained with tartrate-resistant acid phosphatase. 3. Osteoclastogenesis was evaluated using the osteoclast markers CD51, matrix metalloproteinase (MMP)-9 and cathepsin K. At 0.01 μg/mL, (99)Tc-MDP significantly inhibited RANKL-induced osteoclastogenesis without any cytotoxicity. In addition, (99)Tc-MDP abolished the appearance of multinucleated osteoclasts. 4. Real-time RT-PCR analysis of transcription factor expression revealed that (99)Tc-MDP inhibited the expression of c-Fos and nuclear factor of activated T cells. In addition, (99)Tc-MDP inhibited the expression of the inflammatory factors interleukin (IL)-6, tumour necrosis factor-α and IL-1β. Finally, (99)Tc-MDP inhibited the activation of mitogen-activated protein kinases in RAW264.7 cells following RANKL stimulation. 5. In conclusion, (99)Tc-MDP possesses anti-osteoclastogenic activity against RANKL-induced osteoclast formation.

Authors+Show Affiliations

Immunology and Reproductive Biology Laboratory, Medical School and State Key Laboratory of Pharmaceutical Biotechnology, Nanjing University, Nanjing, China.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

23013134

Citation

Gong, Wei, et al. "Technetium-99 Conjugated With Methylene Diphosphonate Inhibits Receptor Activator of Nuclear factor-κB Ligand-induced Osteoclastogenesis." Clinical and Experimental Pharmacology & Physiology, vol. 39, no. 10, 2012, pp. 886-93.
Gong W, Dou H, Liu X, et al. Technetium-99 conjugated with methylene diphosphonate inhibits receptor activator of nuclear factor-κB ligand-induced osteoclastogenesis. Clin Exp Pharmacol Physiol. 2012;39(10):886-93.
Gong, W., Dou, H., Liu, X., Sun, L., & Hou, Y. (2012). Technetium-99 conjugated with methylene diphosphonate inhibits receptor activator of nuclear factor-κB ligand-induced osteoclastogenesis. Clinical and Experimental Pharmacology & Physiology, 39(10), 886-93. https://doi.org/10.1111/j.1440-1681.2012.12006.x
Gong W, et al. Technetium-99 Conjugated With Methylene Diphosphonate Inhibits Receptor Activator of Nuclear factor-κB Ligand-induced Osteoclastogenesis. Clin Exp Pharmacol Physiol. 2012;39(10):886-93. PubMed PMID: 23013134.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Technetium-99 conjugated with methylene diphosphonate inhibits receptor activator of nuclear factor-κB ligand-induced osteoclastogenesis. AU - Gong,Wei, AU - Dou,Huan, AU - Liu,Xianqin, AU - Sun,Lingyun, AU - Hou,Yayi, PY - 2012/9/28/entrez PY - 2012/9/28/pubmed PY - 2013/5/17/medline SP - 886 EP - 93 JF - Clinical and experimental pharmacology & physiology JO - Clin Exp Pharmacol Physiol VL - 39 IS - 10 N2 - 1. In the present study, we investigated the effects of technetium-99 conjugated with methylene diphosphonate ((99)Tc-MDP), an agent used in radionuclide therapy, on receptor activator of nuclear factor-κB ligand (RANKL)-induced osteoclastogenesis and explored the underlying mechanisms. 2. The murine macrophage cell line RAW264.7 and bone marrow-derived-macrophages from C57BL/6 mice (BMM) were used as models for osteoclastogenesis in vitro. The expression of some key factors in RANKL (50 ng/mL)-induced osteoclastogenesis in RAW264.7 cells was investigated by flow cytometry and real-time reverse transcription-polymerase chain reaction (RT-PCR). To detect multinucleated osteoclast formation, RAW264.7 cells were induced with RANKL for 4 days, whereas BMM were induced by 50 ng/mL RANKL and 20 ng/mL macrophage colony-stimulating factor for 7 days, before being stained with tartrate-resistant acid phosphatase. 3. Osteoclastogenesis was evaluated using the osteoclast markers CD51, matrix metalloproteinase (MMP)-9 and cathepsin K. At 0.01 μg/mL, (99)Tc-MDP significantly inhibited RANKL-induced osteoclastogenesis without any cytotoxicity. In addition, (99)Tc-MDP abolished the appearance of multinucleated osteoclasts. 4. Real-time RT-PCR analysis of transcription factor expression revealed that (99)Tc-MDP inhibited the expression of c-Fos and nuclear factor of activated T cells. In addition, (99)Tc-MDP inhibited the expression of the inflammatory factors interleukin (IL)-6, tumour necrosis factor-α and IL-1β. Finally, (99)Tc-MDP inhibited the activation of mitogen-activated protein kinases in RAW264.7 cells following RANKL stimulation. 5. In conclusion, (99)Tc-MDP possesses anti-osteoclastogenic activity against RANKL-induced osteoclast formation. SN - 1440-1681 UR - https://www.unboundmedicine.com/medline/citation/23013134/Technetium_99_conjugated_with_methylene_diphosphonate_inhibits_receptor_activator_of_nuclear_factor_κB_ligand_induced_osteoclastogenesis_ L2 - https://doi.org/10.1111/j.1440-1681.2012.12006.x DB - PRIME DP - Unbound Medicine ER -