scholarly journals Analysis of the Direct and Indirect Effects of Nanoparticle Exposure on Microglial and Neuronal Cells In Vitro

2020 ◽  
Vol 21 (19) ◽  
pp. 7030
Author(s):  
Jasna Lojk ◽  
Lea Babič ◽  
Petra Sušjan ◽  
Vladimir Boštjan Bregar ◽  
Mojca Pavlin ◽  
...  
Keyword(s):  
Indirect Effects ◽  
Neuronal Cells ◽  
Microglial Cells ◽  
Exposure Model ◽  
Direct And Indirect Effects ◽  
Health Related ◽  
Stress Mediators ◽  
The Brain ◽  
Direct Toxicity

Environmental or biomedical exposure to nanoparticles (NPs) can results in translocation and accumulation of NPs in the brain, which can lead to health-related problems. NPs have been shown to induce toxicity to neuronal cells through several direct mechanisms, but only a few studies have also explored the indirect effects of NPs, through consequences due to the exposure of neighboring cells to NPs. In this study, we analysed possible direct and indirect effects of NPs (polyacrylic acid (PAA) coated cobalt ferrite NP, TiO2 P25 and maghemite NPs) on immortalized mouse microglial cells and differentiated CAD mouse neuronal cells in monoculture (direct toxicity) or in transwell co-culture system (indirect toxicity). We showed that although the low NP concentrations (2–25 µg/mL) did not induce changes in cell viability, cytokine secretion or NF-κB activation of microglial cells, even low NP concentrations of 10 µg/mL can affect the cells and change their secretion of protein stress mediators. These can in turn influence neuronal cells in indirect exposure model. Indirect toxicity of NPs is an important and not adequately assessed mechanism of NP toxicity, since it not only affects cells on the exposure sites, but through secretion of signaling mediators, can also affect cells that do not come in direct contact with NPs.

scholarly journals Effect of memantine, an anti-Alzheimer’s drug, on rodent microglial cells in vitro

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Toru Murakawa-Hirachi ◽  
Yoshito Mizoguchi ◽  
Masahiro Ohgidani ◽  
Yoshinori Haraguchi ◽  
Akira Monji
Keyword(s):  
Neuronal Death ◽  
Phagocytic Activity ◽  
Microglial Cell ◽  
Cell Function ◽  
Microglial Cells ◽  
Phagocytosis Assay ◽  
Intracellular Ca ◽  
Β Amyloid ◽  
The Brain

AbstractThe pathophysiology of Alzheimer’s disease (AD) is related to neuroinflammatory responses mediated by microglia. Memantine, an antagonist of N-methyl-d-aspartate (NMDA) receptors used as an anti-Alzheimer’s drug, protects from neuronal death accompanied by suppression of proliferation and activation of microglial cells in animal models of AD. However, it remains to be tested whether memantine can directly affect microglial cell function. In this study, we examined whether pretreatment with memantine affects intracellular NO and Ca2+ mobilization using DAF-2 and Fura-2 imaging, respectively, and tested the effects of memantine on phagocytic activity by human β-Amyloid (1–42) phagocytosis assay in rodent microglial cells. Pretreatment with memantine did not affect production of NO or intracellular Ca2+ elevation induced by TNF in rodent microglial cells. Pretreatment with memantine also did not affect the mRNA expression of pro-inflammatory (TNF, IL-1β, IL-6 and CD45) or anti-inflammatory (IL-10, TGF-β and arginase) phenotypes in rodent microglial cells. In addition, pretreatment with memantine did not affect the amount of human β-Amyloid (1–42) phagocytosed by rodent microglial cells. Moreover, we observed that pretreatment with memantine did not affect 11 major proteins, which mainly function in the phagocytosis and degradation of β-Amyloid (1–42), including TREM2, DAP12 and neprilysin in rodent microglial cells. To the best of our knowledge, this is the first report to suggest that memantine does not directly modulate intracellular NO and Ca2+ mobilization or phagocytic activity in rodent microglial cells. Considering the neuroinflammation hypothesis of AD, the results might be important to understand the effect of memantine in the brain.

Keep Your Brain Tissue Healthy

2021 ◽  
pp. 27-66
Author(s):  
Charles Alessi ◽  
Larry W. Chambers ◽  
Muir Gray
Keyword(s):  
Physical Activity ◽  
Immune System ◽  
Inflammatory Response ◽  
Stress Reduction ◽  
Indirect Effects ◽  
Cognitive Abilities ◽  
Direct And Indirect Effects ◽  
The Impact ◽  
The Brain

This chapter starts by advising how to reduce the impact of stress. When stress becomes long term, the immune system becomes less sensitive to cortisol, and since inflammation is partly regulated by this hormone, this decreased sensitivity heightens the inflammatory response and allows inflammation to get out of control, increasing our risk of many diseases. You can reduce your stress yourself through a variety of methods, including physical activity and mindfulness-based stress reduction. Adequate sleep is also a major factor that can improve cognitive abilities and reduce the risk of dementia, and this chapter outlines what we need to know about sleep cycles, insomnia, and sleep disordered breathing, and how to sleep more and sleep better. The chapter then covers how to protect your brain from over medication (polypharmacy). It finishes by discussing how to maintain and indeed increase your levels of physical activity, and how increasing physical activity has both direct and indirect effects on the brain.

Herbicidal Effects on Crownvetch Rhizobia and Nodule Activity

Weed Science ◽  
1986 ◽  
Vol 34 (3) ◽  
pp. 338-343 ◽  
Author(s):  
John Cardina ◽  
Nathan L. Hartwig ◽  
Felix L. Lukezic
Keyword(s):  
Carbon Dioxide ◽  
Exchange Rate ◽  
Bacterial Growth ◽  
Indirect Effects ◽  
Carbon Dioxide Exchange ◽  
N Fixation ◽  
Intact Plants ◽  
Coronilla Varia ◽  
Direct Toxicity

Two strains of crownvetch (Coronilla variaL. # CZRVA) rhizobia were cultured in vitro with various rates of atrazine [6-chloro-N-ethyl-N′-(1-methylethyl)-1,3,5-triazine-2,4-diamine] and bifenox [methyl 5-(2,4-dichlorophenoxy)-2-nitrobenzoate]. Growth, measured turbidimetrically over 48 h, was similar for both strains. Atrazine and bifenox significantly reduced bacterial growth after 14 and 36 h, respectively, only at the highest concentrations tested (463 μM atrazine and 292 μM bifenox). Since growth of crownvetch rhizobia was apparently not affected by rates of atrazine or bifenox above reasonable soil solution concentrations, it is likely that herbicidal effects on nodulation were due to toxicity to the host plant rather than toxicity to these bacteria. In a growth chamber experiment, total nodule activity (TNA) and carbon dioxide exchange rate (CER) were measured simultaneously in an effort to distinguish direct atrazine effects on nodule function from indirect effects due to inhibition of photosynthesis and a resulting decrease in photosynthate supply to nodules. When 5 and 50 mg atrazine per kg soil were applied to intact plants, CER was severely reduced within 24 h, but similar reductions in TNA were not observed until 48 h after treatment. Total nodule activity was reduced similarly by atrazine and defoliation; the application of atrazine to defoliated plants did not inhibit TNA more than did defoliation alone. The data indicate that reductions in crownvetch nodule activity by atrazine are due to inhibition of photosynthesis or other processes rather than direct toxicity to N fixation.

scholarly journals Direct and Indirect Effects of Androgens on Survival of Hematopoietic Progenitor Cells In Vitro

2005 ◽  
Vol 20 (3) ◽  
pp. 409 ◽  
Author(s):  
Seong-Woo Kim ◽  
Jin-Hee Hwang ◽  
Jae-Min Cheon ◽  
Nam-Sook Park ◽  
Sang-Eun Park ◽  
...  
Keyword(s):  
Progenitor Cells ◽  
Indirect Effects ◽  
Hematopoietic Progenitor Cells ◽  
Direct And Indirect Effects ◽  
Hematopoietic Progenitor

In vitro models to study the direct and indirect effects of HIV-1 infection of the human brain

1994 ◽  
Vol 35 (S1) ◽  
pp. S22-S22
Author(s):  
Monique E. Dubois-Dalcq ◽  
Jia Min Zhou ◽  
Susan Wilt
Keyword(s):  
Human Brain ◽  
Indirect Effects ◽  
In Vitro Models ◽  
Direct And Indirect Effects ◽  
Hiv 1

scholarly journals DIRECT AND INDIRECT EFFECTS OF X-RADIATION ON ANTIBODY-PRODUCING CELLS

1957 ◽  
Vol 105 (5) ◽  
pp. 417-424 ◽  
Author(s):  
Frank J. Dixon ◽  
James C. Roberts ◽  
William O. Weigle
Keyword(s):  
Antibody Response ◽  
Indirect Effects ◽  
Lymphoid Tissue ◽  
Radiation Injury ◽  
Inhibitory Effect ◽  
Significant Inhibition ◽  
Lymphoid Cells ◽  
Whole Body ◽  
Direct And Indirect Effects

X-radiation appears to exert its inhibitory effect on the antibody response by two mutually dependent routes: (a) direct radiation injury to the antibody-producing lymphoid tissue, and (b) indirect effects of altered homeostasis in the radiated host on antibody-producing tissues. Neither of these two effects alone produces significant inhibition of the secondary antibody response made by transferred lymphoid cells. However, 400 to 500 r administered in vitro to the transferred cells, plus 400 r whole body x-radiation of the recipient prior to transfer, completely inhibited the antibody response.

Direct and indirect effects of leptin on preadipocyte proliferation and differentiation

2006 ◽  
Vol 290 (6) ◽  
pp. R1557-R1564 ◽  
Author(s):  
Blair Wagoner ◽  
Dorothy B. Hausman ◽  
Ruth B. S. Harris
Keyword(s):  
Adipose Tissue ◽  
Conditioned Medium ◽  
Indirect Effects ◽  
Leptin Receptor ◽  
Cell Number ◽  
Direct And Indirect Effects ◽  
Sprague Dawley ◽  
Proliferation And Differentiation

Leptin has been shown to reduce body fat in vivo. Adipocytes express the leptin receptor; therefore, it is realistic to expect a direct effect of leptin on adipocyte growth and metabolism. In vitro studies examining the effect of leptin on adipocyte metabolism require supraphysiological doses of the protein to see a decrease in lipogenesis or stimulation of lipolysis, implying an indirect action of leptin. It also is possible that leptin reduces adipose mass by inhibiting preadipocyte proliferation (increase in cell number) and/or differentiation (lipid filling). Thus we determined direct and indirect effects of leptin on preadipocyte proliferation and differentiation in vitro. We tested the effect of leptin (0–500 ng/ml), serum from leptin-infused rats (0.25% by volume), and adipose tissue-conditioned medium from leptin-infused rats (0–30% by volume) on preadipocyte proliferation and differentiation in a primary culture of cells from male Sprague-Dawley rat adipose tissue. Leptin (50 ng/ml) stimulated proliferation of preadipocytes ( P < 0.05), but 250 and 500 ng leptin/ml inhibited proliferation of both preadipocyte and stromal vascular cell fractions ( P < 0.01), as measured by [3H]thymidine incorporation. Serum from leptin-infused rats inhibited proliferation of the adipose and stromal vascular fractions ( P = 0.01), but adipose tissue-conditioned medium had no effect on proliferation of either cell fraction. None of the treatments changed preadipocyte differentiation as measured by sn-glycerophosphate dehydrogenase activity. These results suggest that leptin could inhibit preadipocyte proliferation by modifying release of a factor from tissue other than adipose tissue.

Sign in / Sign up

Export Citation Format

Share Document