Osteopontin directly modulates cytokine expression of primary microglia and increases their survival

Rabenstein, Monika; Vay, Sabine Ulrike; Flitsch, Lea Jessica; Fink, Gereon R.; Schroeter, Michael; Rueger, Maria Adele

doi:10.1016/j.jneuroim.2016.09.009

Cited by 44 publications

(59 citation statements)

References 49 publications

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“…However, after stimulation with LPS at 10 mg/ml, cotreatment with OPN did not reduce the number of iNOS-positive cells. The same result was reflected in the research about NO, suggesting a dose-dependent effect of OPN on LPS-induced NO-release from primary microglia [54]. …”

Section: The Effect Of Opn On Microgliasupporting

confidence: 74%

“…They found that the number of microglial cells in the test group was 100-fold higher than that of the control. And the dead microglia visibly decreased with treatment of 6.25 μ g/ml or 12.5 μ g/ml OPN, which indicated that the appropriate concentration of OPN could increase the survival of microglia under stress conditions [54]. And they speculated that OPN might enhance microglia survival under the stress of nutrient deprivation after cerebral ischemia, which supports the notion that OPN serves as an important regulatory protein of neuroinflammation.…”

Section: The Effect Of Opn On Microgliamentioning

confidence: 79%

“…Ki67-mRNA was quantitatively assessed after OPN treatment using real-time quantitative polymerase chain reaction (RT-qPCR). Microglia treated with OPN at 6.25 μ g/ml for 24 hours or 72 hours did not contain more Ki67-mRNA than untreated microglia, suggesting that OPN had no effect on microglia proliferation [54]. …”

Section: The Effect Of Opn On Microgliamentioning

confidence: 99%

“…In the experiment of Rabenstein et al, microglia were treated with OPN at 6.25 or 12.5 μ g/ml for 24 hours and then zymosan microbeads were added for 2 hours to subsequently quantify phagocytic activity photometrically. The amount of microbeads phagocytosed by microglia was unaffected by OPN treatment compared to untreated control cells, suggesting the phagocytic activity of microglia did not affected by OPN [54], while Tambuyzer et al proposed that freshly harvested microglia initially had a high phagocytic activity, on which OPN treatment had no significant effect. After 24 hours of culture in the DMEM complete medium, their phagocytic activity was reduced to 40% of this initial level.…”

Section: The Effect Of Opn On Microgliamentioning

confidence: 99%

“…Intracellular OPN and hyaluronic acid-CD44-ERM combined into a complex change the cytoskeleton to promote cell movement [58]. However, Rabenstein et al found that OPN did not affect microglia migration by using a modified Boyden chamber transwell migration assay [54]. …”

Section: The Effect Of Opn On Microgliamentioning

confidence: 99%

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The Effect of Osteopontin on Microglia

Liu

Zhong

2017

BioMed Research International

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Osteopontin (OPN) is a proinflammatory cytokine that can be secreted from many cells, including activated macrophages and T-lymphocytes, and is widely distributed in many tissues and cells. OPN, a key factor in tissue repairing and extracellular matrix remodeling after injury, is a constituent of the extracellular matrix of the central nervous system (CNS). Recently, the role of OPN in neurodegenerative diseases has gradually caused widespread concern. Microglia are resident macrophage-like immune cells in CNS and play a vital role in both physiological and pathological conditions, including restoring the integrity of the CNS and promoting the progression of neurodegenerative disorders. Microglia's major function is to maintain homeostasis and the normal function of the CNS, both during development and in response to CNS injury. Although the functional mechanism of OPN in CNS neurodegenerative diseases has yet to be fully elucidated, most studies suggest that OPN play a role in pathogenesis of neurodegenerative diseases or in neuroprotection by regulating the activation and function of microglia. Here, we summarize the functions of OPN on microglia in response to various stimulations in vitro and in vivo.

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Section: The Effect Of Opn On Microgliasupporting

confidence: 74%

Section: The Effect Of Opn On Microgliamentioning

confidence: 79%

Section: The Effect Of Opn On Microgliamentioning

confidence: 99%

Section: The Effect Of Opn On Microgliamentioning

confidence: 99%

Section: The Effect Of Opn On Microgliamentioning

confidence: 99%

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The Effect of Osteopontin on Microglia

Liu

Zhong

2017

BioMed Research International

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Osteopontin regulates proliferation, migration, and survival of astrocytes depending on their activation phenotype

Vay

Olschewski

Petereit

et al. 2021

J of Neuroscience Research

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The glycoprotein osteopontin is highly upregulated in central nervous system (CNS) disorders such as ischemic stroke. Osteopontin regulates cell growth, cell adhesion, homeostasis, migration, and survival of various cell types. Accordingly, osteopontin is considered an essential regulator of regeneration and repair in the ischemic milieu. Astrocytes are the most abundant cells in the CNS and play significant roles in health and disease. Astrocytes are involved in homeostasis, promote neuroprotection, and regulate synaptic plasticity. Upon activation, astrocytes may adopt different phenotypes, termed A1 and A2. The direct effects of osteopontin on astrocytes, especially in distinct activation states, are yet unknown. The current study aimed to elucidate the impact of osteopontin on resting and active astrocytes. We established an inflammatory in vitro model of activated (A1) primary astrocytes derived from neonatal wistar rats by exposure to a distinct combination of proinflammatory cytokines. To model ischemic stroke in vitro, astrocytes were subjected to oxygen and glucose deprivation (OGD) in the presence or absence of osteopontin. Osteopontin modulated the activation phenotype by attenuating A1‐ and restoring A2‐marker expression without compromising the active astrocytes’ immunocompetence. Osteopontin promoted the proliferation of active and the migration of resting astrocytes. Following transient OGD, osteopontin mitigated the delayed ongoing death of primary astrocytes, promoting their survival. Data suggest that osteopontin differentially regulates essential functions of resting and active astrocytes and confirm a significant regulatory role of osteopontin in an in vitro ischemia model. Furthermore, the data suggest that osteopontin constitutes a promising target for experimental therapies modulating neuroregeneration and repair.

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Comparing RNA‐sequencing datasets from astrocytes, oligodendrocytes, and microglia in multiple sclerosis identifies novel dysregulated genes relevant to inflammation and myelination

Drake

Zaman

Simas

et al. 2023

WIREs Mechanisms of Disease

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Central nervous system (CNS) inflammation is a key factor in multiple sclerosis (MS). Invasion of peripheral immune cells into the CNS resulting from an unknown signal or combination of signals results in activation of resident immune cells and the hallmark feature of the disease: demyelinating lesions. These lesion sites are an amalgam of reactive peripheral and central immune cells, astrocytes, damaged and dying oligodendrocytes, and injured neurons and axons. Sustained inflammation affects cells directly located within the lesion site and further abnormalities are apparent diffusely throughout normal-appearing white matter and grey matter. It is only relatively recently, using animal models, new tissue sampling techniques, and next-generation sequencing, that molecular changes occurring in CNS resident cells have been broadly captured. Advances in cell isolation through Fluorescence Activated Cell Sorting (FACS) and laser-capture microdissection together with the emergence of single-cell sequencing have enabled researchers to investigate changes in gene expression in astrocytes, microglia, and oligodendrocytes derived from animal models of MS as well as from primary patient tissue. The contribution of some dysregulated pathways has been followed up in individual studies; however, corroborating results often go unreported between sequencing studies. To this end, we have consolidated results from numerous RNA-sequencing studies to identify and review novel patterns of differentially regulated genes and pathways occurring within CNS glial cells in MS.

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Osteopontin directly modulates cytokine expression of primary microglia and increases their survival

Cited by 44 publications

References 49 publications

The Effect of Osteopontin on Microglia

The Effect of Osteopontin on Microglia

Osteopontin regulates proliferation, migration, and survival of astrocytes depending on their activation phenotype

Comparing RNA‐sequencing datasets from astrocytes, oligodendrocytes, and microglia in multiple sclerosis identifies novel dysregulated genes relevant to inflammation and myelination

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