ArticleThe American journal of pathology2008
Age-related changes in bone morphology are accelerated in group VIA phospholipase A2 (iPLA2beta)-null mice.
Article in The American journal of pathology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
36 citing papers in PubMed, 62 citations in OpenAlex.
- iPLA2β-null mice exposed to natural pathogens exhibit hepatocellular fibrotic injury with male-biased alteration of glycerolipid metabolism.Frontiers in immunology · 2026Article
- 37-Day microgravity exposure in 16-Week female C57BL/6J mice is associated with bone loss specific to weight-bearing skeletal sites.PloS one · 2025Article
- Targeting miR-29 mitigates skeletal senescence and bolsters therapeutic potential of mesenchymal stromal cells.Cell reports. Medicine · 2024Article
- CaProstaglandins & other lipid mediators · 2022Article
- Transcriptomic alterations underline aging of osteogenic bone marrow stromal cells.World journal of stem cells · 2021Article
- How To Build a Bone: PHOSPHO1, Biomineralization, and Beyond.JBMR plus · 2019Review
- Lipoquality control by phospholipase AProceedings of the Japan Academy. Series B, Physical and biological sciences · 2017Review
- Article
- Deficiency of Group VIA Phospholipase A2 (iPLA2β) Renders Susceptibility for Chemical-Induced Colitis.Digestive diseases and sciences · 2015Article
- Calcium-independent phospholipases A2 and their roles in biological processes and diseases.Journal of lipid research · 2015Review
- Article
- Global Inactivation of the Pla2g6 Gene in Mice Does Not Cause Dyslipidemia under Chow or High-fat Diet Conditions.Journal of cancer prevention · 2013Article
- Article
- Phospholipases of mineralization competent cells and matrix vesicles: roles in physiological and pathological mineralizations.International journal of molecular sciences · 2013Article
- Eicosanoids in metabolic syndrome.Advances in pharmacology (San Diego, Calif.) · 2013Review
- Mitochondrial dysfunction and β-cell failure in type 2 diabetes mellitus.Experimental diabetes research · 2012Review
- Phospholipase A2 enzymes: physical structure, biological function, disease implication, chemical inhibition, and therapeutic intervention.Chemical reviews · 2011Review
- Neuroaxonal dystrophy in calcium-independent phospholipase A2β deficiency results from insufficient remodeling and degeneration of mitochondrial and presynaptic membranes.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2011Article
- Random mutagenesis of the mouse genome: a strategy for discovering gene function and the molecular basis of disease.American journal of physiology. Gastrointestinal and liver physiology · 2011Review
- Aging and bone.Journal of dental research · 2010Review
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
Phospholipases A(2) (PLA(2)) hydrolyze the sn-2 fatty acid substituent, such as arachidonic acid, from phospholipids, and arachidonate metabolites are recognized mediators of bone modeling. We have previously generated knockout (KO) mice lacking the group VIA PLA(2) (iPLA(2)beta), which participates in a variety of signaling events; iPLA(2)beta mRNA is expressed in bones of wild-type (WT) but not KO mice. Cortical bone size, trabecular bone volume, bone mineralizing surfaces, and bone strength are similar in WT and KO mice at 3 months and decline with age in both groups, but the decreases are more pronounced in KO mice. The lower bone mass phenotype observed in KO mice is not associated with an increase in osteoclast abundance/activity or a decrease in osteoblast density, but is accompanied by an increase in bone marrow fat. Relative to WT mice, undifferentiated bone marrow stromal cells (BMSCs) from KO mice express higher levels of PPAR-gamma and lower levels of Runx2 mRNA, and this correlates with increased adipogenesis and decreased osteogenesis in BMSCs from these mice. In summary, our studies indicate that age-related losses in bone mass and strength are accelerated in iPLA(2)beta-null mice. Because adipocytes and osteoblasts share a common mesenchymal stem cell origin, our findings suggest that absence of iPLA(2)beta causes abnormalities in osteoblast function and BMSC differentiation and identify a previously unrecognized role of iPLA(2)beta in bone formation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.