ArticleMediators of inflammation2014
Osteopontin expression in the brain triggers localized inflammation and cell death when immune cells are activated by pertussis toxin.
Article in Mediators of inflammation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 11 citations in OpenAlex.
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- Neuroinflammatory Profiling in SIV-Infected Chinese-Origin Rhesus Macaques on Antiretroviral Therapy.Viruses · 2022Article
- LncRNA-XIST Promotes Proliferation and Migration in ox-LDL Stimulated Vascular Smooth Muscle Cells through miR-539-5p/SPP1 Axis.Oxidative medicine and cellular longevity · 2022Article
- Potential Progression Mechanism and Key Genes in Early Stage of mTBI.Evidence-based complementary and alternative medicine : eCAM · 2022Article
- Osteopontin counters human immunodeficiency virus type 1-induced impairment of neurite growth through mammalian target of rapamycin and beta-integrin signaling pathways.Journal of neurovirology · 2019Article
- Review
- Peripheral and central neuronal ATF3 precedes CD4+ T-cell infiltration in EAE.Experimental neurology · 2016Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Upregulation of osteopontin (OPN) is a characteristic of central nervous system pathologies. However, the role of OPN in inflammation is still controversial, since it can both prevent cell death and induce the migration of potentially damaging inflammatory cells. To understand the role of OPN in inflammation and cell survival, we expressed OPN, utilizing an adenoviral vector, in the caudoputamen of mice deficient in OPN, using beta-galactosidase- (β-gal-) expressing vector as control. The tissue pathology and the expression of proinflammatory genes were compared in both treatments. Interestingly, inflammatory infiltrate was only found when the OPN-vector was combined with a peripheral treatment with pertussis toxin (Ptx), which activated peripheral cells to express the OPN receptor CD44v6. Relative to β-gal, OPN increased the levels of inflammatory markers, including IL13Rα1, CXCR3, and CD40L. In Ptx-treated OPN KOs, apoptotic TUNEL+ cells surrounding the OPN expression site increased, compared to β-gal. Together, these results show that local OPN expression combined with a peripheral inflammatory stimulus, such as Ptx, may be implicated in the development of brain inflammation and induction of cell death, by driving a molecular pattern characteristic of cytotoxicity. These are characteristics of inflammatory pathologies of the CNS in which OPN upregulation is a hallmark.
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