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R 7050

Manufactured by Santa Cruz Biotechnology
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Sourced in United States

R-7050 is a laboratory instrument designed for cell culture applications. It is a multifunction incubator that provides precise control of temperature, humidity, and CO2 levels to support the growth and maintenance of cell lines.

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Lab products found in correlation

Dimethyl sulphoxide, by Merck Group (2 mentions) Dba 2, by Charles River Laboratories (2 mentions) High phosphate diet, by Altromin (2 mentions) Etanercept, by Pfizer (2 mentions) 5 6 dichloro 1 β d ribofuranosylbenzimidazole drb, by Cayman Chemical (1 mentions) Tnf α, by Thermo Fisher Scientific (1 mentions)

4 protocols using r 7050

1

TNFα Regulation of Endothelial Cells

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Human endothelial cells were treated with TNFα (PeproTech, Hamburg, Germany, #300-01A) for the times indicated in the results section. Preliminary concentration response experiments revealed 10 ng/mL TNFα as an optimal concentration with a maximum effect on ACE expression and low cell toxicity. For wash out experiments, cells were washed twice with basal MCDB131 medium and further cultured in normal growth medium (without TNFα). The TNFα receptor was inhibited by pretreatment with R-7050 (10 μmol/L) from Santa Cruz (Dallas/Texas, USA, CAS#303997-35-5) 30 minutes prior to stimulation. For the RNA stability assay, cells were pretreated with the RNA polymerase II inhibitor 5,6-dichloro-1-β-D-ribofuranosylbenzimidazole (DRB; 20 μg/mL; Cayman Chemical, Ann Arbor/Michigan, USA, CAS#53-85-0) two hours prior to stimulation. RG-108 (30 μmol/L; Active Motif, La Hulpe, Belgium, #14104) was used to inhibit DNMT. The p38 mitogen activated protein kinase inhibitor; SB202190 was from Calbiochem (Darmstadt, Germany).
Mudersbach T., Siuda D., Kohlstedt K, & Fleming I. (2019). Epigenetic control of the angiotensin-converting enzyme in endothelial cells during inflammation. PLoS ONE, 14(5), e0216218.
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2

Murine Model of Vascular Calcification

Cited 1 time
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Female 8-week-old dilute-brown agouti 2 (DBA/2NCrl, hereafter referred to as DBA/2) mice were obtained from Charles River (Sulzfeld, Germany) and housed in a virus/antibody-free environment. These mice have an inherent susceptibility to high-phosphate diet-triggered calcification [15 (link), 16 (link)]. To induce media calcification, they were placed on high-phosphate diet (Altromin, Germany) containing 20.2 g phosphorus, 9.4 g calcium, 0.7 g magnesium and 500 IU vitamin D3 per kg. The standard chow contained 7.0 g phosphorus, 10.0 g calcium, 2.2 g magnesium and 1000 IU vitamin D3 per kg. Mice were then followed for 5–14 days and culled under anaesthesia. For the interventional studies, DBA/2 mice were divided into three treatment groups to receive vehicle control (dimethylsulphoxide; Sigma, St. Louis, MO), TNFα inhibitor etanercept (Pfizer, New York, NY) at a dose of 10 mg/kg body weight, or TNFα receptor antagonist R-7050 (Santa Cruz, Dallas, TX) at a dose of 6 mg/kg body weight, respectively [17 (link)]. These drugs were applied via intraperitoneal injections every alternate day. All animal experiments were approved by Austrian veterinary authorities (BMWF-66.010/0047-II/3b/2012) and corresponded to directive 2010/63/EU of the European Parliament.
Kirsch A.H., Kirsch A., Artinger K., Schabhüttl C., Goessler W., Klymiuk I., Gülly C., Fritz G.A., Frank S., Wimmer R., Brodmann M., Anders H.J., Pramstaller P.P., Rosenkranz A.R., Eller K, & Eller P. (2015). Heterogeneous susceptibility for uraemic media calcification and concomitant inflammation within the arterial tree. Nephrology Dialysis Transplantation, 30(12), 1995-2005.
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3

DBA/2 Mouse Model of Vascular Calcification

Cited 1 time
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Female 8-week-old dilute-brown agouti 2 (DBA/2NCrl, hereafter referred to as DBA/2) mice were obtained from Charles River (Sulzfeld, Germany) and housed in a virus/antibody-free environment. These mice have an inherent susceptibility to high-phosphate diet-triggered calcification [15 (link),16 (link)]. To induce media calcification, they were placed on high-phosphate diet (Altromin, Germany) containing 20.2 g phosphorus, 9.4 g calcium, 0.7 g magnesium and 500 IU vitamin D3 per kg. The standard chow contained 7.0 g phosphorus, 10.0 g calcium, 2.2 g magnesium and 1000 IU vitamin D3 per kg. Mice were then followed for 5–14 days and culled under anaesthesia. For the interventional studies, DBA/2 mice were divided into three treatment groups to receive vehicle control (dimethylsulphoxide; Sigma, St. Louis, MO), TNFα inhibitor etanercept (Pfizer, New York, NY) at a dose of 10 mg/kg body weight, or TNFα receptor antagonist R-7050 (Santa Cruz, Dallas, TX) at a dose of 6 mg/kg body weight, respectively [17 (link)]. These drugs were applied via intraperitoneal injections every alternate day. All animal experiments were approved by Austrian veterinary authorities (BMWF-66.010/0047-II/3b/2012) and corresponded to directive 2010/63/EU of the European Parliament.
Kirsch A.H., Kirsch A., Artinger K., Schabhüttl C., Goessler W., Klymiuk I., Gülly C., Fritz G.A., Frank S., Wimmer R., Brodmann M., Anders H.J., Pramstaller P.P., Rosenkranz A.R., Eller K, & Eller P. (2015). Heterogeneous susceptibility for uraemic media calcification and concomitant inflammation within the arterial tree. Nephrology Dialysis Transplantation, 30(12), 1995-2005.
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4

Nitroglycerine-Induced Trigeminal Pain Model

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Mice received i.p. injection of NTG or vehicle solution at a 10 ml/kg volume. NTG (American Regent, Shirley, NY) in a stock solution (5 mg/ml) was freshly diluted with 0.9% saline to a dose of 10 mg/kg. We conducted microinjection of R-7050 (0.5 µl, 0.1 mM in 0.9% saline; Santa Cruz Biotechnology, Inc.) into bilateral spinal trigeminal nucleus caudalis (Sp5C) using a Hamilton syringe at 30 min prior to NTG injection or 1 day after NTG. Intra-Sp5C injection of R-7050 or saline was performed at 0.25 µl/min and the needle was remained in place for additional three minutes. At the end of experiments, the microinjection site was confirmed histologically.
Tang Y., Liu S., Shu H., Yanagisawa L, & Tao F. (2019). Gut microbiota dysbiosis enhances migraine-like pain via TNFα upregulation. Molecular neurobiology, 57(1), 461-468.
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