Beta-cryptoxanthin stimulates apoptotic cell death and suppresses cell function in osteoclastic cells: change in their related gene expression

Journal of Cellular Biochemistry
Satoshi Uchiyama, Masayoshi Yamaguchi

Abstract

The effect of beta-cryptoxanthin, a kind of carotenoid, on osteoclastic cells in mouse marrow culture system in vitro was investigated. The macrophage colony-stimulating factor (M-CSF)-dependent bone marrow macrophages were cultured in the presence of M-CSF (10 ng/ml) and receptor activator of NF-kappaB ligand (RANKL; 25 ng/ml) for 4 days. The osteoclastic cells formed were further cultured in medium containing either vehicle or beta-cryptoxanthin (10(-8)-10(-6) M) with or without M-CSF (10 ng/ml) and RANKL (50 ng/ml) for 24-72 h. Osteoclastic cells were significantly decreased with culture of beta-cryptoxanthin (10(-7) or 10(-6) M) with or without M-CSF and RANKL for 24, 48, or 72 h. beta-Cryptoxanthin (10(-8) M)-induced decrease in osteoclastic cells were significantly inhibited in the presence of caspase-3 inhibitor (10(-8) or 10(-7) M). Agarose gel electrophoresis showed the presence of low-molecular-weight deoxyribonucleic acid (DNA) fragments of adherent cells cultured with beta-cryptoxanthin (10(-7) or 10(-6) M) for 24 or 48 h, indicating that the carotenoid induces apoptotic cell death. Apoptosis-related gene expression was determined using reverse transcription-polymerase chain reaction (RT-PCR). Culture with beta-cryp...Continue Reading

References

Mar 1, 1996·Bone·J P BonjourR Rizzoli
Nov 26, 1999·The Journal of Nutrition·C M RohdeH F DeLuca
Aug 7, 2002·Journal of Bone and Mineral Research : the Official Journal of the American Society for Bone and Mineral Research·Joanne H E PromislowElizabeth Barrett-Connor
Aug 29, 2002·Hepatology : Official Journal of the American Association for the Study of Liver Diseases·Anne-Marie PreauxPhilippe Mavier
Feb 6, 2004·Biological & Pharmaceutical Bulletin·Satoshi UchiyamaMasayoshi Yamaguchi
Mar 12, 2004·Biochemical Pharmacology·Satoshi Uchiyama, Masayoshi Yamaguchi
Mar 20, 2004·Molecular and Cellular Biochemistry·Masayoshi Yamaguchi, Satoshi Uchiyama
Jun 5, 2004·Journal of Bone and Mineral Research : the Official Journal of the American Society for Bone and Mineral Research·Toru OgasawaraHiroshi Kawaguchi
Dec 28, 2004·Journal of Bone and Mineral Research : the Official Journal of the American Society for Bone and Mineral Research·Xiaojun WuJay M McDonald
Jun 18, 2005·Journal of Cellular Biochemistry·Satoshi Uchiyama, Masayoshi Yamaguchi
Sep 6, 2005·Biological & Pharmaceutical Bulletin·Satoshi Uchiyama, Masayoshi Yamaguchi

❮ Previous
Next ❯

Citations

Apr 5, 2012·Journal of Biomedical Science·Masayoshi Yamaguchi
Jul 24, 2012·Regenerative Medicine·Kevin W-H LoCato T Laurencin
Jan 10, 2016·Nutrition Reviews·Betty J BurriChenghao Zhu
Aug 26, 2009·Journal of Clinical Periodontology·Gerard J LindenFrank Kee
Mar 5, 2013·Archives of Oral Biology·Masaru NishigakiNarisato Kanamura
Apr 5, 2007·Journal of Cellular Biochemistry·Paula H Stern
Oct 26, 2018·Journal of Bone and Mineral Metabolism·Gustavo Ribeiro OliveiraKarina Fittipaldi Bombonato-Prado
Jan 23, 2020·Journal of Clinical Medicine·Yurie KurokawaMichihiro Mutoh
Nov 2, 2006·Yakugaku zasshi : Journal of the Pharmaceutical Society of Japan·Masayoshi Yamaguchi

❮ Previous
Next ❯

Related Concepts

Related Feeds

BCL-2 Family Proteins

BLC-2 family proteins are a group that share the same homologous BH domain. They play many different roles including pro-survival signals, mitochondria-mediated apoptosis and removal or damaged cells. They are often regulated by phosphorylation, affecting their catalytic activity. Here is the latest research on BCL-2 family proteins.

Apoptotic Caspases

Apoptotic caspases belong to the protease enzyme family and are known to play an essential role in inflammation and programmed cell death. Here is the latest research.

Apoptosis

Apoptosis is a specific process that leads to programmed cell death through the activation of an evolutionary conserved intracellular pathway leading to pathognomic cellular changes distinct from cellular necrosis