The suitability of BV2 cells as alternative model system for primary microglia cultures or for animal experiments examining brain inflammation

Henn, Anja; Lund, Søren Peter; Hedtjärn, Maj; Schrattenholz, Andreé; Pörzgen, Peter; Leist, Marcel

doi:10.14573/altex.2009.2.83

Cited by 636 publications

(522 citation statements)

References 59 publications

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“…Inspired by these observations, we studied the effect of nimodipine on microglia in greater detail using two different microglia cell lines (N9 and BV-2). These two cell lines were chosen because their calcium signaling, cytokine production, and cell-cell interactions were reported to be comparable to primary cells (22,23). By applying different doses of nimodipine to N9 and BV-2 cultures for 24 h, we were able to detect a dose-dependent loss of cells.…”

Section: Resultsmentioning

confidence: 99%

Nimodipine fosters remyelination in a mouse model of multiple sclerosis and induces microglia-specific apoptosis

Schampel

Volovitch

Koeniger

et al. 2017

Proc. Natl. Acad. Sci. U.S.A.

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Despite continuous interest in multiple sclerosis (MS) research, there is still a lack of neuroprotective strategies, because the main focus has remained on modulating the immune response. Here we performed in-depth analysis of neurodegeneration in experimental autoimmune encephalomyelitis (EAE) and in in vitro studies regarding the effect of the well-established L-type calcium channel antagonist nimodipine. Nimodipine treatment attenuated clinical EAE and spinal cord degeneration and promoted remyelination. Surprisingly, we observed calcium channel-independent effects on microglia, resulting in apoptosis. These effects were cell-type specific and irrespective of microglia polarization. Apoptosis was accompanied by decreased levels of nitric oxide (NO) and inducible NO synthase (iNOS) in cell culture as well as decreased iNOS and reactive oxygen species levels in EAE. In addition, increased numbers of Olig2 + APC + oligodendrocytes were detected. Overall, nimodipine application seems to generate a favorable environment for regenerative processes and therefore could be a treatment option for MS, because it combines features of immunomodulation with beneficial effects on neuroregeneration.M ultiple sclerosis (MS) is the most prevalent neurological disease of the CNS in young adults and is characterized by inflammation, demyelination, and axonal pathology (1) that result in multiple neurological and cognitive deficits (1-3). Intensive MS research studies have investigated modulating the immune system (4). Common therapeutic strategies are effective in slowing disease progression and attenuating the symptoms, but they cannot cure the disease. The option of preventing neurodegeneration early on would be a valuable addendum to customary treatment (4). Here we suggest that application of nimodipine could be an elegant way to target both neuroinflammation and neurodegeneration. The dihydropyridine nimodipine is commonly known as a 1.2 voltagegated L-type calcium channel antagonist and is used to treat hypertension and other cardiovascular diseases (5, 6). It also is used to prevent vasospasms after subarachnoidal hemorrhage (5) because of its high affinity for the CNS (7-9). Current research trials are examining its effects on brain injury, epilepsy, cognitive performance, and behavioral effects (6,7,10,11). Its influence on oxidative stress, neuronal survival, synaptic plasticity, and aging also are being investigated, especially within the hippocampus (10, 12). In addition, it was recently shown that the risk of suffering from Parkinson's disease was decreased under treatment with dihydropyridines (13). These studies suggest that nimodipine might have beneficial effects in MS as well, although its role in neurodegenerative diseases that are mediated by inflammatory events has not been well established (6). So far, nimodipine-mediated effects in the CNS have been claimed to result mainly from the modulation of neuronal activity, and studies on the potential effects of nimodipine on (micro)glia have not yet been conduct...

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Section: Resultsmentioning

confidence: 99%

Nimodipine fosters remyelination in a mouse model of multiple sclerosis and induces microglia-specific apoptosis

Schampel

Volovitch

Koeniger

et al. 2017

Proc. Natl. Acad. Sci. U.S.A.

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“…The involvement of microglia in neurodegenerative process of diseases was evidenced in many studies using BV2 microglia cell line [46,47]. The effect of BSA samples on BV2 cell viability was evaluated by using MTT assays and FACS.…”

Section: Resultsmentioning

confidence: 99%

Deciphering metal-induced oxidative damages on glycated albumin structure and function

Baraka-Vidot¹,

Navarra

Leone

et al. 2014

Biochimica et Biophysica Acta (BBA) - General Subjects

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Background: Metal ions such as copper or zinc are involved in the development of neurodegenerative pathologies and metabolic diseases such as diabetes mellitus. Albumin structure and functions are impaired following metaland glucose-mediated oxidative alterations. The aim of this study was to elucidate effects of Cu(II) and Zn(II) ions on glucose-induced modifications in albumin by focusing on glycation, aggregation, oxidation and functional aspects. Methods: Aggregation and conformational changes in albumin were monitored by spectroscopy, fluorescence and microscopy techniques. Biochemical assays such as carbonyl, thiol groups, albumin-bound Cu, fructosamine and amine group measurements were used. Cellular assays were used to gain functional information concerning antioxidant activity of oxidized albumins. Results: Both metals promoted inhibition of albumin glycation associated with an enhanced aggregation and oxidation process. Metal ions gave rise to the formation of β-amyloid type aggregates in albumin exhibiting impaired antioxidant properties and toxic activity to murine microglia cells (BV2). The differential efficiency of both metal ions to inhibit albumin glycation, to promote aggregation and to affect cellular physiology is compared. Conclusions and general significance: Considering the key role of oxidized protein in pathology complications, glycation-mediated and metal ion-induced impairment of albumin properties might be important parameters to be followed and fought.

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“…1A). To next examine the function of LRP1 in the phagocytosis of CNS myelin debris, we repeated necrotic cell internalization experiments using the microglial cell line BV2 as model phagocytes and the oligodendrocyte cell line N20.1 as model necrotic cells (34,42). When BV2 were pretreated with GST-RAP, phagocytosis of necrotic oligodendrocytes was inhibited by 35% (p Ͻ 0.001, n ϭ 6; Fig.…”

Section: Resultsmentioning

confidence: 99%

Identification of the Low Density Lipoprotein (LDL) Receptor-related Protein-1 Interactome in Central Nervous System Myelin Suggests a Role in the Clearance of Necrotic Cell Debris

Fernández-Castañeda

Arandjelovic

Stiles

et al. 2013

Journal of Biological Chemistry

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Background: LRP1 is a scavenger receptor involved in the clearance of apoptotic cells and myelin vesicles. Results: Novel ligands for LRP1 were discovered in CNS myelin by affinity purification combined with proteomics. Conclusion: Some ligands are intracellular proteins, suggesting a function for LRP1 in the clearance of necrotic debris. Significance: LRP1 mediates the removal of cellular waste and could maintain homeostasis.

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The suitability of BV2 cells as alternative model system for primary microglia cultures or for animal experiments examining brain inflammation

Cited by 636 publications

References 59 publications

Nimodipine fosters remyelination in a mouse model of multiple sclerosis and induces microglia-specific apoptosis

Nimodipine fosters remyelination in a mouse model of multiple sclerosis and induces microglia-specific apoptosis

Deciphering metal-induced oxidative damages on glycated albumin structure and function

Identification of the Low Density Lipoprotein (LDL) Receptor-related Protein-1 Interactome in Central Nervous System Myelin Suggests a Role in the Clearance of Necrotic Cell Debris

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