ArticleThe American journal of pathology2010
Progressive secondary neurodegeneration and microcalcification co-occur in osteopontin-deficient mice.
Article in The American journal of pathology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 23 citations in OpenAlex.
- Osteopontin Regulates AQP4 Expression by TRPV4 Activation in Müller Cells: Implications for Retinal Homeostasis.Molecular neurobiology · 2025Article
- Inorganic phosphate exporter heterozygosity in mice leads to brain vascular calcification, microangiopathy, and microgliosis.Brain pathology (Zurich, Switzerland) · 2023Article
- Intracranial calcification in Fam20c-deficient mice recapitulates human Raine syndrome.Neuroscience letters · 2023Article
- Astrocytes are involved in the formation of corpora amylacea-like structures from neuronal debris in the CA1 region of the rat hippocampus after ischemia.Frontiers in cellular neuroscience · 2023Article
- Osteopontin mediates the formation of corpora amylacea-like structures from degenerating neurons in the CA1 region of the rat hippocampus after ischemia.Cell and tissue research · 2022Article
- Microglia shield the murine brain from damage mediated by the cytokines IL-6 and IFN-α.Frontiers in immunology · 2022Article
- Microglia control small vessel calcification via TREM2.Science advances · 2021Article
- Results from Phase I Clinical Trial with Intraspinal Injection of Neural Stem Cells in Amyotrophic Lateral Sclerosis: A Long-Term Outcome.Stem cells translational medicine · 2019Article
- Osteopontin and its spatiotemporal relationship with glial cells in the striatum of rats treated with mitochondrial toxin 3-nitropropionic acid: possible involvement in phagocytosis.Journal of neuroinflammation · 2019Article
- The Retina of Osteopontin deficient Mice in Aging.Molecular neurobiology · 2018Article
- Spatiotemporal expression of osteopontin in the striatum of rats subjected to the mitochondrial toxin 3-nitropropionic acid correlates with microcalcification.Scientific reports · 2017Article
- Article
- Spinal but not cortical microglia acquire an atypical phenotype with high VEGF, galectin-3 and osteopontin, and blunted inflammatory responses in ALS rats.Neurobiology of disease · 2014Article
- PDGF, pericytes and the pathogenesis of idiopathic basal ganglia calcification (IBGC).Brain pathology (Zurich, Switzerland) · 2014Review
- Sustained expression of osteopontin is closely associated with calcium deposits in the rat hippocampus after transient forebrain ischemia.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2012Article
- Senescence-accelerated Mice (SAMs) as a Model for Brain Aging and Immunosenescence.Aging and disease · 2011Article
Corrections and comments
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Authors and funding
7 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In the brain, osteopontin (OPN) may function in a variety of pathological conditions, including neurodegeneration, microcalcification, and inflammation. In this study, we addressed the role of OPN in primary and secondary neurodegeneration, microcalcification, and inflammation after an excitotoxic lesion by examining OPN knock-out (KO) mice. Two, four, and ten weeks after injection of the glutamate analogue ibotenate into the corticostriatal boundary, the brains of 12 mice per survival time and strain were evaluated. OPN was detectable in neuron-shaped cells, in microglia, and at the surface of dense calcium deposits. At this primary lesion site, although the glial reaction was attenuated in OPN-KO mice, lesion size and presence of microcalcification were comparable between OPN-KO and wild-type mice. In contrast, secondary neurodegeneration at the thalamus was more prominent in OPN-KO mice, and this difference increased over time. This was paralleled by a dramatic rise in the regional extent of dense microcalcification. Despite these differences, the numbers of glial cells did not significantly differ between the two strains. This study demonstrates for the first time a genetic model with co-occurrence of neurodegeneration and microcalcification, mediated by the lack of OPN, and suggests a basic involvement of OPN action in these conditions. In the case of secondary retrograde or transneuronal degeneration, OPN may have a protective role as intracellular actor.
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