Phosphatidylcholine metabolism and choline kinase in human osteoblasts

Biochim Biophys Acta. 2014 Jun;1841(6):859-67. doi: 10.1016/j.bbalip.2014.02.004. Epub 2014 Feb 25.

Abstract

There is a paucity of information about phosphatidylcholine (PC) biosynthesis in bone formation. Thus, we characterized PC metabolism in both primary human osteoblasts (HOB) and human osteosarcoma MG-63 cells. Our results show that the CDP-choline pathway is the only de novo route for PC biosynthesis in both HOB and MG-63 cells. Both CK activity and CKα expression in MG-63 cells were significantly higher than those in HOB cells. Silencing of CKα in MG-63 cells had no significant effect on PC concentration but decreased the amount of phosphocholine by approximately 80%. The silencing of CKα also reduced cell proliferation. Moreover, pharmacological inhibition of CK activity impaired the mineralization capacity of MG-63 cells. Our data suggest that CK and its product phosphocholine are required for the normal growth and mineralization of MG-63 cells.

Keywords: Choline kinase; MG-63 cells; Mineralization; Phosphatidylcholine; Phosphocholine; Proliferation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Calcification, Physiologic / genetics*
  • Cell Line, Tumor
  • Cell Proliferation / drug effects
  • Choline Kinase / antagonists & inhibitors
  • Choline Kinase / genetics*
  • Choline Kinase / metabolism
  • Hemicholinium 3 / pharmacology
  • Humans
  • Lipid Metabolism / genetics
  • Osteoblasts / enzymology
  • Osteogenesis / genetics*
  • Phosphatidylcholines / biosynthesis*
  • Phosphatidylcholines / genetics
  • Phosphatidylcholines / metabolism
  • RNA, Small Interfering

Substances

  • Phosphatidylcholines
  • RNA, Small Interfering
  • Hemicholinium 3
  • Choline Kinase