Impact of calcium-independent phospholipase A2 beta (iPLA2� | 8151
Journal of Glycomics & Lipidomics

Journal of Glycomics & Lipidomics
Open Access

ISSN: 2153-0637

Impact of calcium-independent phospholipase A2 beta (iPLA2β) on differentiation and activity of calvarial bone-derived osteoblasts

2nd International Conference and Expo on Lipids: Metabolism, Nutrition & Health

October 03-05, 2016 Orlando, USA

William Hancock, Amjad Javed and Sasanka Ramanadham

University of Alabama at Birmingham, USA

Scientific Tracks Abstracts: J Glycomics Lipidomics

Abstract :

Bone modeling is modulated by lipid signals, especially arachidonic acid and its metabolites. These lipid signals can be generated by phospholipases A2 which hydrolyze the sn-2 fatty acid substituent from membrane phospholipids; cellular AA is esterified in this position within membrane glycerophospholipids. Knockout mice lacking the group VIA calcium-independent phospholipases A2 beta (iPLA2�?²) exhibited an enhanced, age-related decline in cortical bone size, trabecular bone volume and bone mineralizing surfaces. They also revealed a dramatic decrease in mineral apposition rate by 6-months of age and accelerated age-related lipid droplet accumulation in their bone marrow. Current studies demonstrated that osteoblasts from calvaria of iPLA2�?²-knockout mice express lower levels of Runx2, bone morphogenetic protein 2 and alkaline phosphatase mRNA, relative to WT osteoblasts. These findings correlate with decreased osteoblastogenesis and osteoblast activity, as reflected by reduced mineralization determined by Alizarin red staining and quantification. This reduction can be rescued by the treatment of osteoblasts with arachidonic acid and prostaglandin E2, a cyclooxygenase-catalyzed metabolite of arachidonic acid, which was hydrolyzed through activation of iPLA2�?². Prostaglandin E2 was known to increase osteoblast replication and differentiation. Our studies indicated that induction of differentiation factors and bone mineralization occur, in part, by activation of iPLA2�?² and subsequent generation of iPLA2�?²-derived lipid signals. These findings indicated a prominent role for iPLA2�?² in determining mesenchymal stem cell fate, bone maintenance and bone remodeling.

Biography :

William Hancock has completed his PhD from the University of Alabama at Birmingham School of Medicine in the Department of Cell, Developmental, and Integrative Biology. Utilizing an undergraduate background in Physics, he is pursuing a wider understanding of the impact of potent lipid derived signals in the control of transcriptional events related to Physiology and Pathophysiology.