Mwreg30

Manufactured by BD

Sourced in United States

The MWReg30 is a laboratory instrument designed for microwave digestion and extraction applications. It provides precise temperature and pressure control for efficient sample preparation. The core function of the MWReg30 is to facilitate the rapid and effective breakdown of various sample matrices using microwave energy.

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Lab products found in correlation

Mec13, by BD (5 mentions) Rat anti mouse f4 80 primary antibody, by BD (2 mentions) Anti hexon polyclonal antibody, by Abcam (2 mentions) 4 6 diamidino 2 phenylindole (dapi), by Merck Group (2 mentions) 7 aminoactinomycin d 7 aad, by Thermo Fisher Scientific (2 mentions) Facsaria 2, by BD (2 mentions) Alexa fluor 488, by Thermo Fisher Scientific (2 mentions) F4 80, by Bio-Rad (1 mentions) Cd45r b220, by BD (1 mentions) Magnetic activated cell sorting (macs), by Miltenyi Biotec (1 mentions) Recombinant tpo, by Thermo Fisher Scientific (1 mentions) Sdf 1, by Thermo Fisher Scientific (1 mentions) Epidermal growth factor (egf), by Thermo Fisher Scientific (1 mentions) Bc 5300, by Mindray (1 mentions) Kx 21n, by Sysmex (1 mentions) Hoechst, by Merck Group (1 mentions) Cd140b, by BioLegend (1 mentions) Ab7778, by R&D Systems (1 mentions) Ab34710, by Abcam (1 mentions) Cryojane system, by Leica Biosystems (1 mentions)

20 protocols using mwreg30

Platelet Depletion in Mice

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Mice were administered anti-mouse CD41 antibody (clone MWReg30; BD Pharmingen) to selectively deplete platelets or IgG1 (to act as a control) via intraperitoneal injection every 48 hours for up to 4 weeks (duration was dependent on the experiment). Concentration of anti-CD41 or IgG1 ranged between 0.2 and 0.4 mg/kg as indicated in Figure 1. As described previously, antibody dose escalation was necessary to maintain thrombocytopenia over time.^{34 (link)} In our study, 0.2 mg/kg anti-CD41 was sufficient to maintain thrombocytopenia for the first 2 weeks, followed by an increase of 0.1 mg/kg per week thereafter.

Herd O.J., Rani G.F., Hewitson J.P., Hogg K., Stone A.P., Cooper N., Kent D.G., Genever P.G, & Hitchcock I.S. (2021). Bone marrow remodeling supports hematopoiesis in response to immune thrombocytopenia progression in mice. Blood Advances, 5(23), 4877-4889.

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Comprehensive Phenotyping of PIKfyvefl/fl Pf4-Cre Mice

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Necropsies were performed on approximately 50 control mice and 50 PIKfyve^fl/fl Pf4-Cre mice between 3 weeks and 28 weeks of age. They included macroscopic observations, body and organ weight measurements, complete blood counts, serum chemistry analysis, and microscopic examination of the brain, thymus, lymph nodes, heart, lung, small intestine, large intestine, liver, spleen, pancreas, kidney, ovaries, testis, skin, muscle, fat, and bone marrow. Fresh postmortem tissues were fixed overnight in 10% formalin, paraffin-embedded, sectioned, and stained with hematoxylin/eosin, PAS, Alcian Blue, and Trichrome Mason. Frozen tissue sections were fixed with formalin for 5 minutes and stained for oil red O. For immunohistochemistry, frozen tissue sections were fixed with 4% paraformaldehyde for 5 minutes, and stained with F4/80 (Serotec; 1:100), CD41 (BD Pharmingen; MWReg30; 1:50), and CD45R/B220 (BD Pharmingen; RA3–6B2; 1:500). For X-gal staining, frozen tissue sections were fixed with 0.5% glutaraldehyde for 10 minutes, and stained overnight with the chromogenic substrate for β-galactosidase, X-gal (Cell Center, University of Pennsylvania).

Min S.H., Suzuki A., Stalker T.J., Zhao L., Wang Y., McKennan C., Riese M.J., Guzman J.F., Zhang S., Lian L., Joshi R., Meng R., Seeholzer S.H., Choi J.K., Koretzky G., Marks M.S, & Abrams C.S. (2014). Loss of PIKfyve in platelets causes a lysosomal disease leading to inflammation and thrombosis in mice. Nature communications, 5, 4691.

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Hematopoietic Differentiation of Flk1+ and VEcad+ Cells

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MACS (Miltenyi) sorted Flk1⁺ cells from day 4 EBs (over 95% purity) were cultured on confluent OP9s in MEMα supplemented with 10% FCS. Mesodermal colonies were allowed to form for 36 h before dox was added. Haematopoietic cells were not seen before this time point. After 48 h, cells were fixed in 2% PFA overnight, blocked, stained with purified CD41 antibody (BD Biosciences, 553847, MWReg30), visualised by DAB staining, and mesodermal colonies containing (at least two) small rounded budding CD41⁺ haematopoietic cells were scored. Specific staining was confirmed using an isotype control antibody. VEcad⁺ cells from day 6 EBs were sorted using a BD Influx and plated on confluent OP9s, and cultured for 4 days in MEMα supplemented with 10% FCS. After 4 days, cells were fixed and stained as above using purified CD31 antibody (BD Biosciences, 553370, MEC13.3), and endothelial sheet colonies were scored.

Wilkinson A.C., Kawata V.K., Schütte J., Gao X., Antoniou S., Baumann C., Woodhouse S., Hannah R., Tanaka Y., Swiers G., Moignard V., Fisher J., Hidetoshi S., Tijssen M.R., de Bruijn M.F., Liu P, & Göttgens B. (2014). Single-cell analyses of regulatory network perturbations using enhancer-targeting TALEs suggest novel roles for PU.1 during haematopoietic specification. Development (Cambridge, England), 141(20), 4018-4030.

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Platelet Depletion and Inhibition

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To induce thrombocytopenia, mice were injected R.O. with anti-GPIbα platelet-depleting antibody (Emfret Analytics, clone R300) or anti–α_IIbβ₃ integrin antibody (BD Biosciences, clone MWReg30) at 2 μg/g BW. Platelet counts were determined 5 minutes before and 30 minutes after antibody injection, mice were then sacrificed and perfused, and organs were collected for sectioning. To block α_IIbβ₃ function, mice were injected R.O. with 75 μg anti–α_IIbβ₃ F(ab′)₂ antibody (clone 4H5) every 24 hours. Inhibition of α_IIbβ₃ was confirmed using a whole-blood platelet aggregation assay.

Lee R.H., Ghalloussi D., Harousseau G.L., Kenny J.P., Kramer P.A., Proamer F., Nieswandt B., Flick M.J., Gachet C., Casari C., Eckly A, & Bergmeier W. (2022). Rasa3 deficiency minimally affects thrombopoiesis but promotes severe thrombocytopenia due to integrin-dependent platelet clearance. JCI Insight, 7(8), e155676.

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In Vivo Platelet Binding Assay

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Listeria-OVA was labeled with 5 μM CFSEin PBS for 30 min at 37 °C at a density of 1 × 10⁹ CFU per ml. For analysis of in vivo platelet binding, CFSE-labeled Listeria-OVA were used to infect WT or Btla^−/− mice. Blood was collect and immediately diluted 20-fold in flow cytometry buffer (PBS, 0.5% (wt/vol) BSA) containing heparin (50 IU/ml) 1, 5, 60 minutes after infection. Samples were kept at room temperature and manipulated minimally; platelet-specific anti-CD41 (MWReg30; BD Biosciences) was added directly to the sample, followed by dilution of the sample 1:10 in flow cytometry buffer before analysis.

Yang X., Zhang X., Sun Y., Tu T., Fu M.L., Miller M, & Fu Y.X. (2014). A BTLA-mediated bait-and-switch strategy permits Listeria expansion in CD8α+ DCs to promote long term T cell responses. Cell host & microbe, 16(1), 68-80.

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Modulating Platelet Levels for Alveolar Regeneration

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To stimulate thromobopoiesis, recombinant thrombopoietin (TPO) was intraperitoneally injected into Thpo^−/− or WT mice at dose of 25 μg/kg on daily basis ten days before PNX and afterwards. To deplete circulating platelets, rat anti-mouse CD41 monoclonal antibody (BD Biosciences, clone MWReg30) was intraperitoneally injected into mice at dose of 10 mg/kg every three days. Recombinant TPO, EGF, and SDF1 were obtained from Peprotech. Vehicle for individual cytokine was also injected as control group.
The effects of injected cytokine on alveolar regeneration were evaluated with control groups treated with vehicle, including alteration in circulating platelets and parameters of alveologenesis (as described above). In particular, mouse platelets were collected at indicated time points from the retrobulbar venous plexus of anesthetized mice, using heparinized hematocrit tubing. Platelet count in peripheral blood was then determined with automated Advia-120 Hematology System.

Rafii S., Cao Z., Lis R., Siempos I.I., Chavez D., Shido K., Rabbany S.Y, & Ding B.S. (2015). Platelet-derived SDF1 primes pulmonary capillary vascular niche to drive lung alveolar regeneration. Nature cell biology, 17(2), 123-136.

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Platelet Survival Quantification in Mice

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Six- to forty-week-old male mice were used in this study. Platelets from C57BL/6J or IL4R-IbαTg mice were isolated in modified Tyrode's buffer, stained with CFSE as described above, washed once and pooled to 1.5 × 10⁶ μl⁻¹. Platelets were infused right away into recipient C57BL/6J mice (1.5 × 10⁸ platelets per 10 g body weight). After 1 h and every 24 h thereafter, blood was drawn from recipient mice and infused platelets were counted as described above. To measure endogenous survival of IL4R-IbαTg platelets, a single intravenous injection of 5 μg AlexaFluor 488-conjugated anti-GPIX antibody (clone Xia.B4, Emfret analytics) in 100 μl PBS was administered at t=0. Whole blood was drawn after every 24 h, diluted and incubated with a PE-conjugated anti-CD41 antibody (MWReg30, BD Biosciences) for 10 min at room temperature. The ratio of AlexaFluor 488-positive platelets to PE-positive ones was determined.

Deng W., Xu Y., Chen W., Paul D.S., Syed A.K., Dragovich M.A., Liang X., Zakas P., Berndt M.C., Di Paola J., Ware J., Lanza F., Doering C.B., Bergmeier W., Zhang X.F, & Li R. (2016). Platelet clearance via shear-induced unfolding of a membrane mechanoreceptor. Nature Communications, 7, 12863.

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Visualizing Adenovirus Interactions with Kupffer Cells

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Example 12

To analyze Ad interactions with Kupffer cells, 10¹⁰virus particles were injected into the tail vein, and 60 min later, livers were flushed with saline via cardiac perfusion, harvested and immediately frozen in an OCT compound. Frozen liver sections were fixed and stained with rat anti-mouse F4/80 primary antibody (BD Biosciences, San Diego, Calif.) to detect Kupffer cells. Specific binding of primary antibodies was visualized with secondary anti-rat-Alexa Flour 488 antibody (Molecular Probes Inc., Eugene, Oreg.). To detect Ad particles, liver sections were stained with anti-hexon polyclonal antibody (Abcam, Cambridge, Mass.). The staining with biotinilated anti-hexon primary antibody was developed with secondary Cy3-labeled streptavidin. To detect platelets and endothelial cells on liver sections, antibodies to CD41 (platelets, clone MWReg30) or CD31-FITC (endothelial cells, clone MEC13.3 (both from BD Biosciences) were used. Cell nuclei were counterstained with 1 μg/ml 4′,6-diamidino-2-phenylindole (DAPI) (Sigma, St. Louis, Mo.).

US11364306B2. Detargeted adenovirus variants and related methods (2022-06-21). ADCURE BIOTECHNOLOGIES, LLC. [US]. Inventors: Dmitry M. Shayakhmetov [US], Nelson C. Di Paolo [US].

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Induction of Immune Thrombocytopenia in Mice

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ITP mouse model was established as described previously [24 (link), 25 (link)]. In brief, mice were administrated with anti-platelet monoclonal antibody (rat anti-mouse integrin GPIIb/CD41 immunoglobulin, clone MWReg30) (BD Biosciences) intraperitoneally at a dose of 0.1 mg/kg body weight to prepare ITP model. After antibody injection, peripheral whole blood was collected to measure platelet count by an automatic hematology analyzer (BC-5300, Mindray, Shenzhen, China) [24 (link), 25 (link)].

Tong H., Ding Y., Gui X., Sun Z., Wang G., Zhang S., Xu Z., Wang X., Xu X., Ju W., Li Y., Li Z., Zeng L., Xu K, & Qiao J. (2021). Dimethyl fumarate inhibits antibody-induced platelet destruction in immune thrombocytopenia mouse. Thrombosis Journal, 19, 61.

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Experimental Immune Thrombocytopenia Mouse Model

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IVIg (Gamimune N) was purchased from Bayer (Whippany, NJ, USA). Experimental ITP was induced as described previously [18 (link),19 (link),82 (link),83 (link)]. The mice were intravenously injected with 0.1 mg/kg (body weight) of an antiplatelet monoclonal antibody (rat antimouse integrin α_IIb/CD41 Ig, clone MWReg30, BD Biosciences, Franklin Lakes, NJ, USA) to induce ITP. To analyze the platelet count, whole blood samples (100–120 μL) of the mice were collected with an anticoagulant, a citrate dextrose solution (38 mM citric acid, 75 mM sodium citrate, and 100 mM dextrose), in Eppendorf tubes. Subsequently, platelet counts were measured using a hematology analyzer (KX-21N, Sysmex, Kobe, Japan) at various time intervals [77 (link),78 (link),84 (link)]. To investigate the ameliorative effects of intravenous treatment with IVIg (high dose, 2 g/kg; vehicle: saline; injection at 0 h), cold (4 °C) exposure and restraint stress for 9 h was implemented. Anti-CD41 Ig was treated together with these treatments (IVIg, cold, restraint stress).

Li C.C., Munalisa R., Lee H.Y., Lien T.S., Chan H., Hung S.C., Sun D.S., Cheng C.F, & Chang H.H. (2023). Restraint Stress-Induced Immunosuppression Is Associated with Concurrent Macrophage Pyroptosis Cell Death in Mice. International Journal of Molecular Sciences, 24(16), 12877.

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