Neutrophil-mediated cellular cytotoxicity triggered by immobilized aggregated IgG: Anin vitro model of cell injury during immune complex diseases

1984 ◽  
Vol 4 (6) ◽  
pp. 439-444 ◽  
Author(s):  
Franco Dallegri ◽  
Franco Patrone ◽  
Guido Frumento ◽  
Alberto Ballestrero ◽  
Carlo Sacchetti
Keyword(s):  
Immune Complex ◽  
Cell Injury ◽  
Complex Diseases ◽  
Cellular Cytotoxicity ◽  
Vitro Model

scholarly journals An in Vitro Model of Immune Complex-mediated Basement Membrane Zone Separation Caused by Pemphigoid Antibodies, Leukocytes, and Complement

1982 ◽  
Vol 78 (4) ◽  
pp. 285-290 ◽  
Author(s):  
W. Ray Gammon ◽  
Carolyn C. Merritt ◽  
Daniel M. Lewis ◽  
W. Mitchell Sams ◽  
Jaime R. Carlo ◽  
...  
Keyword(s):  
Basement Membrane ◽  
Immune Complex ◽  
In Vitro Model ◽  
Basement Membrane Zone ◽  
Vitro Model

scholarly journals T-2 Toxin Exposure Induces Apoptosis in TM3 Cells by Inhibiting Mammalian Target of Rapamycin/Serine/Threonine Protein Kinase(mTORC2/AKT) to Promote Ca2+Production

2018 ◽  
Vol 19 (11) ◽  
pp. 3360 ◽  
Author(s):  
Ji Wang ◽  
Chenglin Yang ◽  
Zhihang Yuan ◽  
Jine Yi ◽  
Jing Wu
Keyword(s):  
Cell Injury ◽  
Mammalian Target Of Rapamycin ◽  
Annexin V ◽  
Target Of Rapamycin ◽  
Dependent Manner ◽  
Toxin Exposure ◽  
Concentration Changes ◽  
Vitro Model ◽  
Induced Apoptosis

Although mTOR (the mammalian target of rapamycin) can regulate intracellular free Ca2+concentration in normal cultured podocytes, it remains elusive as to how mTORC2/AKT-mediated Ca2+participates in the process of T-2 toxin-induced apoptosis. The potential signaling responsible for intracellular Ca2+ concentration changes was investigated using immunoblot assays in an in vitro model of TM3 cell injury induced by T-2 toxin. Changes in Ca2+ were assessed using the Ca2+-sensitive fluorescent indictor dye Fura 2-AM. The cytotoxicity of TM3 cells was assessed with an MTT bioassay, and apoptosis was measured using Annexin V-FITC staining. Following T-2 toxin treatment, the growth of cells, phospho-mTORSer2481, phospho-mTORSer2448, and phospho-AktSer473 were significantly decreased in a time-dependent manner, whereas Ca2+ and apoptosis were increased. T-2 toxin-induced apoptosis was prevented by BAPTA-AM (a Ca2+chelator) and MHY1485 (an mTOR activator), and the application of mTOR activator MHY1485 also prevented the increase of intracellular free Ca2+concentration in TM3 cells. Our results strongly suggest that T-2 toxin exposure induces apoptosis in TM3 cells by inhibiting mTORC2/AKT to promote Ca2+ production.

Kidney tubular epithelial cell injury in shock wave lithoripsy: The search for an appropriate in vitro model

1995 ◽  
Vol 98 (5) ◽  
pp. 2942-2943
Author(s):  
James A. McAteer ◽  
Andrew P. Evan ◽  
James E. Lingeman ◽  
Sharon P. Andreoli
Keyword(s):  
Shock Wave ◽  
Epithelial Cell ◽  
In Vitro Model ◽  
Cell Injury ◽  
Tubular Epithelial Cell ◽  
Vitro Model ◽  
Epithelial Cell Injury

Detection of complement activation in immune complex diseases: six methods compared.

1986 ◽  
Vol 32 (12) ◽  
pp. 2170-2174 ◽  
Author(s):  
T Sun ◽  
J Stagias
Keyword(s):  
Immune Complex ◽  
Lupus Erythematosus ◽  
Complement Activation ◽  
Complex Diseases ◽  
Renal Diseases ◽  
Good Resolution ◽  
Gram Negative Bacteremia ◽  
Quantitative Results ◽  
Acquired Immunodeficiency ◽  
Immunodeficiency Syndrome

Abstract We compared the performance of six complement tests: electrophoresis, immunofixation, immunoelectrophoresis, and nephelometric quantifications of C3, C4, and C3d. We used 123 blood samples from 60 control subjects and 63 patients with immune complex diseases: systemic lupus erythematosus, idiopathic thrombocytopenic purpura, rheumatoid arthritis, acquired immunodeficiency syndrome, renal diseases, vasculitis, cryoglobulinemia, Gram-negative bacteremia, Hashimoto's thyroiditis, rheumatic heart disease, malaria, and chronic active hepatitis. Immunofixation and quantification of C3d were better for detecting complement activation, their sensitivity rates (90.5% and 89.3%, respectively) being higher than those of the other tests studied. Immunofixation is a relatively simple and inexpensive test, provides good resolution of protein bands, and yields results that are easily quantified with a densitometer. Nephelometry of C3d provides more rapid and accurate quantitative results than immunofixation, but commercial reagents are not yet available. The causes of false-positive results in complement tests and the mechanisms of complement activation in AIDS are also discussed.

scholarly journals No Cytotoxic and Inflammatory Effects of Empagliflozin and Dapagliflozin on Primary Renal Proximal Tubular Epithelial Cells under Diabetic Conditions In Vitro

2020 ◽  
Vol 21 (2) ◽  
pp. 391 ◽  
Author(s):  
Patrick C. Baer ◽  
Benjamin Koch ◽  
Janina Freitag ◽  
Ralf Schubert ◽  
Helmut Geiger
Keyword(s):  
Epithelial Cells ◽  
Cell Injury ◽  
Cellular Damage ◽  
Tubular Epithelial Cells ◽  
Urinary Glucose ◽  
Proximal Tubular Epithelial Cells ◽  
Proximal Tubular ◽  
Vitro Model ◽  
Renal Proximal Tubular

Gliflozins are inhibitors of the renal proximal tubular sodium-glucose co-transporter-2 (SGLT-2), that inhibit reabsorption of urinary glucose and they are able to reduce hyperglycemia in patients with type 2 diabetes. A renoprotective function of gliflozins has been proven in diabetic nephropathy, but harmful side effects on the kidney have also been described. In the current project, primary highly purified human renal proximal tubular epithelial cells (PTCs) have been shown to express functional SGLT-2, and were used as an in vitro model to study possible cellular damage induced by two therapeutically used gliflozins: empagliflozin and dapagliflozin. Cell viability, proliferation, and cytotoxicity assays revealed that neither empagliflozin nor dapagliflozin induce effects in PTCs cultured in a hyperglycemic environment, or in co-medication with ramipril or hydro-chloro-thiazide. Oxidative stress was significantly lowered by dapagliflozin but not by empagliflozin. No effect of either inhibitor could be detected on mRNA and protein expression of the pro-inflammatory cytokine interleukin-6 and the renal injury markers KIM-1 and NGAL. In conclusion, empa- and dapagliflozin in therapeutic concentrations were shown to induce no direct cell injury in cultured primary renal PTCs in hyperglycemic conditions.

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