scholarly journals A functional in vitro model for studies of intracellular motility in digitonin-permeabilized erythrophores.

1982 ◽  
Vol 94 (3) ◽  
pp. 727-739 ◽  
Author(s):  
M E Stearns ◽  
R L Ochs
Keyword(s):  
Small Molecules ◽  
In Vitro Model ◽  
Inhibitory Effects ◽  
High Voltage Electron Microscopy ◽  
Voltage Electron ◽  
Stabilizing Solution ◽  
Vitro Model ◽  
Cytoskeletal Elements ◽  
Intracellular Motility

Phase contrast cine results demonstrate that erythrophores maintain saltatory particle motion for hours after permeabilization with 0.001% digitonin in a cytoskeletal stabilizing solution at 23 degrees C. High voltage electron microscopy (HVEM) studies reveal that cytoskeletal elements are retained intact, except in immediate subplasmalemmal regions where the plasma membrane is punctured by digitonin. During digitonin treatments, cells are permeable to ions, small molecules, and antibodies. We find that motion is Ca2+ and ATP-sensitive, and optimal in PIPES buffer (pH 7.2 containing 1 mM Mg2+/ATP and EGTA-CA2+ (10(-7) M Ca2+) at 37 degrees C. Experiments testing the inhibitory effects of vanadate (0.4-10 microM), ouabain (100-600 microM), N-ethyl maleimide, and the cytochalasins B and D indicate that a dyneinlike ATPase may provide the motive force for driving saltatory pigment motion in erythropores.

scholarly journals β-Naphthoflavone and Ethanol Reverse Mitochondrial Dysfunction in A Parkinsonian Model of Neurodegeneration

2020 ◽  
Vol 21 (11) ◽  
pp. 3955
Author(s):  
Jesus Fernandez-Abascal ◽  
Elda Chiaino ◽  
Maria Frosini ◽  
Gavin P. Davey ◽  
Massimo Valoti
Keyword(s):  
Complex I ◽  
In Vitro Model ◽  
Inhibitory Effects ◽  
Cyp Induction ◽  
Cyp Isoforms ◽  
Vitro Model ◽  
Complex I Activity ◽  
Cyp 2D6

The 1-methyl-4-phenylpyridinium (MPP+) is a parkinsonian-inducing toxin that promotes neurodegeneration of dopaminergic cells by directly targeting complex I of mitochondria. Recently, it was reported that some Cytochrome P450 (CYP) isoforms, such as CYP 2D6 or 2E1, may be involved in the development of this neurodegenerative disease. In order to study a possible role for CYP induction in neurorepair, we designed an in vitro model where undifferentiated neuroblastoma SH-SY5Y cells were treated with the CYP inducers β-naphthoflavone (βNF) and ethanol (EtOH) before and during exposure to the parkinsonian neurotoxin, MPP+. The toxic effect of MPP+ in cell viability was rescued with both βNF and EtOH treatments. We also report that this was due to a decrease in reactive oxygen species (ROS) production, restoration of mitochondrial fusion kinetics, and mitochondrial membrane potential. These treatments also protected complex I activity against the inhibitory effects caused by MPP+, suggesting a possible neuroprotective role for CYP inducers. These results bring new insights into the possible role of CYP isoenzymes in xenobiotic clearance and central nervous system homeostasis.

scholarly journals Beneficial Influence of Platelets on Antibiotic Efficacy in an In Vitro Model of Staphylococcus aureus-Induced Endocarditis

2004 ◽  
Vol 48 (7) ◽  
pp. 2551-2557 ◽  
Author(s):  
Renee-Claude Mercier ◽  
Robert M. Dietz ◽  
Jory L. Mazzola ◽  
Arnold S. Bayer ◽  
Michael R. Yeaman
Keyword(s):  
Staphylococcus Aureus ◽  
In Vitro Model ◽  
Antimicrobial Effect ◽  
Human Platelets ◽  
Inhibitory Effects ◽  
Activated Platelets ◽  
Vitro Model ◽  
Antibiotic Efficacy ◽  
Chamber Fluid

ABSTRACT Platelets contribute to antimicrobial host defense against infective endocarditis (IE) by releasing platelet microbicidal proteins (PMPs). We investigated the influence of thrombin-stimulated human platelets on the evolution of simulated IE in the presence and absence of vancomycin or nafcillin. Staphylococcus aureus strains differing in intrinsic susceptibility to PMPs or antibiotics were studied: ISP479C (thrombin-induced PMP-1 [tPMP-1] susceptible; nafcillin and vancomycin susceptible), ISP479R (tPMP-1 resistant; nafcillin and vancomycin susceptible), and GISA-NJ (tPMP-1 intermediate-susceptible; vancomycin intermediate-susceptible). Platelets were introduced and thrombin activated within the in vitro IE model 30 min prior to inoculation with S. aureus. At 0 to 24 h postinoculation, bacterial densities in chamber fluid and simulated endocardial vegetations (SEVs) were quantified and compared among groups. Activated platelets alone, or in combination with antibiotics, inhibited the proliferation of ISP479C in chamber fluid or SEVs over the initial 4-h period (P < 0.05 versus controls). Moreover, nafcillin-containing regimens exerted inhibitory effects beyond 4 h against ISP479C in both model phases. By comparison, activated platelets inhibited GISA-NJ proliferation in SEVs but not in chamber fluid. The combination of platelets plus nafcillin or vancomycin significantly inhibited proliferation of the GISA-NJ strain in SEVs compared to the effect of platelets or antibiotics alone (P < 0.05). In contrast, platelets did not significantly alter the antistaphylococcal efficacies of nafcillin or vancomycin against ISP479R. These data support our hypothesis that a beneficial antimicrobial effect may result from the interaction among platelets, PMPs, and anti-infective agents against antibiotic-susceptible or -resistant staphylococci that exhibit a tPMP-1-susceptible or -intermediate-susceptible phenotype.

GSK-3 mediates differentiation and activation of proinflammatory dendritic cells

Blood ◽  
2006 ◽  
Vol 109 (4) ◽  
pp. 1584-1592 ◽  
Author(s):  
Elena Rodionova ◽  
Michael Conzelmann ◽  
Eugene Maraskovsky ◽  
Michael Hess ◽  
Michael Kirsch ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
In Vitro Model ◽  
Glycogen Synthase ◽  
Human Monocyte ◽  
Glycogen Synthase Kinase 3 ◽  
Inhibitory Effects ◽  
Tnf Α ◽  
Vitro Model

Abstract The key components of the intracellular molecular network required for the expression of a specific function of dendritic cells (DCs) are as yet undefined. Using an in vitro model of human monocyte-derived DC differentiation, this study investigates the role of glycogen synthase kinase 3 (GSK-3), a multifunctional enzyme critical for cellular differentiation, apoptosis, self-renewal, and motility, in this context. We demonstrate that GSK-3 (1) inhibits macrophage development during differentiation of DCs, (2) is constitutively active in immature DCs and suppresses spontaneous maturation, and (3) acquires a proinflammatory functional status mediating high levels of IL-12, IL-6, and TNF-α secretion, and partially inhibits IL-10 in the context of DC activation. In particular, GSK-3 enhances IL-12p35 mRNA expression and thus the production of the proinflammatory cytokine IL-12p70 by integrating the activities of other kinases priming GSK-3 targets and the inhibitory effects of Akt-1. GSK-3 may therefore act as a key integrator of activating and inhibitory pathways involved in proinflammatory DC differentiation and activation.

Four new triterpenoids from Chisocheton paniculatus and their anti-inflammatory activities

2012 ◽  
Vol 90 (2) ◽  
pp. 199-204 ◽  
Author(s):  
Ming-Hua Yang ◽  
Jun-Song Wang ◽  
Jian-Guang Luo ◽  
Xiao-Bing Wang ◽  
Ling-Yi Kong
Keyword(s):  
Spectroscopic Data ◽  
In Vitro Model ◽  
2D Nmr ◽  
No Production ◽  
Moderate Activity ◽  
Inhibitory Effects ◽  
Raw264.7 Macrophages ◽  
Anti Inflammatory ◽  
Vitro Model

As part of our continuing effort to discover new potential anti-inflammatory agents, four new triterpenoids, chisopanins L-O (1–4), were isolated from the twigs of Chisocheton paniculatus. Their structures were established on the basis of detailed analysis of spectroscopic data, including IR, NMR (1D and 2D NMR), and HR-ESI-MS. Their inhibitory effects against nitric oxide (NO) production were evaluated in an in vitro model of lipopolysaccharide (LPS)-stimulated RAW264.7 macrophages. Compounds 1, 3, and 4 were found to exhibit moderate activity with IC50 values less than 10 μmol/L.

Potent inhibitory effects of steroids in an in vitro model of angiogenesis

1996 ◽  
Vol 150 (3) ◽  
pp. 457-464 ◽  
Author(s):  
D C Jaggers ◽  
W P Collins ◽  
S R Milligan
Keyword(s):  
In Vitro Model ◽  
Ovarian Follicle ◽  
Collagen Gel ◽  
Rat Aorta ◽  
Significant Inhibition ◽  
Inhibitory Effects ◽  
High Concentrations ◽  
Vitro Model ◽  
Very High

Abstract The regulation of angiogenesis in the ovarian follicle and corpus luteum is unclear. Steroids are produced at very high concentrations in these tissues and we therefore examined the effect of steroids on angiogenesis in vitro. Explants of rat aorta were embedded in collagen gel and cultured in serum-free medium. Capillary-like microvessels were produced from the explants and microvessel number and length were measured in the presence and absence of steroids. At a concentration of 10 μg/ml, cortisol, progesterone, 17α-hydroxyprogesterone and medroxyprogesterone acetate produced degeneration of microvessels after 7 days of steroid treatment (P<0·01). Androstenedione and tetrahydro-S-(11-deoxytetrahydro-cortisol) (tetrahydro S) produced degeneration at a slower rate: androstenedione inhibited microvessel growth after 11 days (P<0·01) and tetrahydro S after 14 days (P<0·05). Oestriol had no effect on microvessels; oestrone had a slow degenerative effect with significant inhibition seen after 14 days (P<0·01). Oestradiol-17β at a concentration of 10 μg/ml completely inhibited microvessel growth from the explant cultures (P<0·01) while at 1 μg/ml it caused degenerative effects on growing microvessels. The effects of oestradiol and cortisol were reversible on removal of steroid-containing medium and replacement with 10% serum. We conclude that oestradiol may modulate angiogenesis in tissues in which the steroid concentration is high. Journal of Endocrinology (1996) 150, 457–464

scholarly journals Down-regulation of microRNA-203a suppresses IL-1β-induced inflammation and cartilage degradation in human chondrocytes through Smad3 signaling

2020 ◽  
Vol 40 (3) ◽  
Author(s):  
Yongbo An ◽  
Guang Wan ◽  
Jingang Tao ◽  
Mingxing Cui ◽  
Qinglan Zhou ◽  
...  
Keyword(s):  
Articular Cartilage ◽  
Inflammatory Response ◽  
In Vitro Model ◽  
Joint Inflammation ◽  
Cartilage Degradation ◽  
Inhibitory Effects ◽  
Key Factor ◽  
Ecm Degradation ◽  
Vitro Model

Abstract Osteoarthritis (OA) is a chronic and prevalent degenerative musculoskeletal disorder, which is characterized by articular cartilage degradation and joint inflammation. MicroRNA-203a (miR-203a) has been shown to be involved in multiple pathological processes during OA, but little is known about its function in chondrocyte extracellular matrix (ECM) degradation. In the present study, we aimed to elucidate the effects of miR-203a on articular cartilage degradation and joint inflammation. We observed that the miR-203a level was significantly up-regulated in OA tissues and in an in vitro model of OA, respectively. Inhibition of miR-203a significantly alleviated the interleukin (IL)-1β-induced inflammatory response and ECM degradation in chondrocytes. Moreover, mothers against decapentaplegic homolog 3 (Smad3), a key factor in maintaining chondrocyte homeostasis, was identified as a putative target of miR-203a in chondrocytes. More importantly, inhibition of Smad3 impaired the inhibitory effects of the miR-203a on IL-1β-induced inflammatory response and ECM degradation. Collectively, these results demonstrated that miR-203a may contribute to articular cartilage degradation of OA by targeting Smad3, suggesting a novel therapeutic target for the treatment of OA.

An in vitro model for investigation of vitamin A effects on wound healing

2021 ◽  
pp. 1-6
Author(s):  
Hoda Keshmiri Neghab ◽  
Mohammad Hasan Soheilifar ◽  
Gholamreza Esmaeeli Djavid
Keyword(s):  
Wound Healing ◽  
Endothelial Cell ◽  
Vitamin A ◽  
In Vitro Model ◽  
Cellular Proliferation ◽  
Endothelial Cell Migration ◽  
Normal Fibroblast ◽  
Anti Inflammatory ◽  
Vitro Model

Abstract. Wound healing consists of a series of highly orderly overlapping processes characterized by hemostasis, inflammation, proliferation, and remodeling. Prolongation or interruption in each phase can lead to delayed wound healing or a non-healing chronic wound. Vitamin A is a crucial nutrient that is most beneficial for the health of the skin. The present study was undertaken to determine the effect of vitamin A on regeneration, angiogenesis, and inflammation characteristics in an in vitro model system during wound healing. For this purpose, mouse skin normal fibroblast (L929), human umbilical vein endothelial cell (HUVEC), and monocyte/macrophage-like cell line (RAW 264.7) were considered to evaluate proliferation, angiogenesis, and anti-inflammatory responses, respectively. Vitamin A (0.1–5 μM) increased cellular proliferation of L929 and HUVEC (p < 0.05). Similarly, it stimulated angiogenesis by promoting endothelial cell migration up to approximately 4 fold and interestingly tube formation up to 8.5 fold (p < 0.01). Furthermore, vitamin A treatment was shown to decrease the level of nitric oxide production in a dose-dependent effect (p < 0.05), exhibiting the anti-inflammatory property of vitamin A in accelerating wound healing. These results may reveal the therapeutic potential of vitamin A in diabetic wound healing by stimulating regeneration, angiogenesis, and anti-inflammation responses.

Präsidentenposter: Regulation der Expression der β-Defensine hBD-2 und hBD-3 in einem in vitro Model der Candida Ösophagitis: NF-κB, MAPK/AP-1 und EGFR

2009 ◽  
Vol 47 (09) ◽  
Author(s):  
N Steubesand ◽  
K Kiehne ◽  
R Pahl ◽  
G Brunke ◽  
UR Fölsch ◽  
...  
Keyword(s):  
In Vitro Model ◽  
Vitro Model
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