Apoe b6.129p2 apoetm1unc j

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ApoE-/- (B6.129P2-Apoetm1Unc/J) is a mouse strain with a targeted mutation in the apolipoprotein E (Apoe) gene, resulting in the lack of functional ApoE protein. This mouse model is commonly used in research related to lipid metabolism and atherosclerosis.

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14 protocols using apoe b6.129p2 apoetm1unc j

Apo-E and miR-155 Knockout Mice in Diet-Induced Atherosclerosis

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All animal experiments were performed in accordance with the Institutional Animal Care and Use Committee (IACUC) guidelines and were approved by the IACUC of Lewis Katz School of Medicine (LKSOM) at Temple University. Apolipoprotein E (ApoE, B6.129P2-ApoE^tm1Unc/J, stock no. 002052) knockout mice, microRNA-155 (miR-155, B6.Cg-Mir155^tm1Rsky/J, stock no. 007745) knockout mice, and wild-type (WT) mice were of a C57BL/6J background, and were purchased from the Jackson Laboratory (Bar Harbor, ME, United States). Mice were housed under controlled conditions in the LKSOM Animal Facility, where they had ad libitum access to standard chow diet/HFD, water, and were subject to a 12-h light-dark cycle. DKO mice were generated as previously reported (11 (link)) by crossing ApoE^-/- mice with miR155^-/- mice. Mice were age-matched and gender-specific in all experiment groups, unless otherwise stated. At eight weeks old, mice either remained on normal chow diet (10.7% fat, 23.9% protein, 5.1% fiber, 58.7% carbohydrate/other, 200ppm cholesterol; Labdiet 5001) or switched to HFD [20% (w/w) fat, 17.4% protein, 5% fiber, 49.9% carbohydrate/other, 2027 ppm cholesterol (0.15% (w/w) cholesterol); TestDiet AIN-76A] (34 (link)) for 12 weeks or 24 weeks, specified in each experiment.

Johnson C., Drummer IV C., Shan H., Shao Y., Sun Y., Lu Y., Saaoud F., Xu K., Nanayakkara G., Fang P., Bagi Z., Jiang X., Choi E.T., Wang H, & Yang X. (2021). A Novel Subset of CD95+ Pro-Inflammatory Macrophages Overcome miR155 Deficiency and May Serve as a Switch From Metabolically Healthy Obesity to Metabolically Unhealthy Obesity. Frontiers in Immunology, 11, 619951.

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ApoE-/- Mice Bone Marrow Chimeras

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Snails infected with S. mansoni (strain NMRI, NR-21962) were provided by the Schistosome Research Reagent Resource Center for distribution by BEI Resources, NIAID NIH. ApoE^-/- (B6.129P2-Apoetm1Unc/J) were purchased from the Jackson Laboratories and bred at the University of Utah. 6-8-week-old male mice were housed in pathogen-free conditions and were fed standard rodent chow (2019 rodent chow, Harlan Teklad) until 10–14 days before infection when they were transitioned to a high-fat diet (HFD: 21% milk fat, 0.15% cholesterol: TD 88137 Envigo). Bone marrow chimeras were generated by treating male ApoE^-/- mice that had been on high- fat diet for 4 weeks with 20mg/kg of pharmaceutical grade busulfan for 5 days (total dose of 100mg/kg). On day 6 mice were i.v. injected with 2.5–3 x 10⁶ bone marrow cells from either 10-week S. mansoni infected or control uninfected ApoE^-/- mice on high-fat diet. Reconstitution was validated via flow-cytometry at 3-weeks post-transfer and recipient mice were maintained on high-fat diet for 10-weeks post-reconstitution.

Cortes-Selva D., Gibbs L., Maschek J.A., Nascimento M., Van Ry T., Cox J.E., Amiel E, & Fairfax K.C. (2021). Metabolic reprogramming of the myeloid lineage by Schistosoma mansoni infection persists independently of antigen exposure. PLoS Pathogens, 17(1), e1009198.

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Mice Strains for Neuroscience Research

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We used female C57BL/6J (WT, n = 162), B6.129S7-Il1r1tm1Imx/J (IL1R1^−/−, n = 28) and apolipoprotein E–deficient (ApoE^−/−; B6.129P2-Apoetm1Unc/J, n = 24) mice aged 8–12 weeks (The Jackson Laboratories, Bar Harbor, ME, USA) for our studies. We also used transgenic mice expressing green fluorescent protein (GFP) under the Nestin-promoter (Nestin-GFP, n = 10)^{26 (link), 27 (link)}. Nestin-GFP mice were a gift from Dr. Grigori Enikolopov (Cold Spring Harbor Laboratory, NY, USA). Age-matched mice were randomly allocated either to control or treatment groups. The study was approved by the Subcommittee on Animal Research Care at Massachusetts General Hospital (Boston, MA).

Sager H.B., Heidt T., Hulsmans M., Dutta P., Courties G., Sebas M., Wojtkiewicz G.R., Tricot B., Iwamoto Y., Sun Y., Weissleder R., Libby P., Swirski F.K, & Nahrendorf M. (2015). Targeting Interleukin-1β Reduces Leukocyte Production After Acute Myocardial Infarction. Circulation, 132(20), 1880-1890.

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Atherosclerosis Progression in ApoE-/- Mice

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C57BL/6 control and Apoe^−/− (B6.129P2-Apoe^tm1Unc/J) mice were purchased from The Jackson Laboratory (Bar Harbor, ME). The Apoe^−/− Ifnαβr^−/− mice, which also have a knockout of the type I IFN receptor, have previously been generated and described by us.^{18 (link)} N-α-benzoyl-N5-(2-chloro-1-iminoethyl)-L-ornithine amide, or Cl-amidine,^{28 (link)} was synthesized as previously described.^{29 (link)} Unless otherwise specified, mice were treated with either Cl-amidine (10 mg/kg/d) or an equal volume of phosphate-buffered saline (PBS) by daily subcutaneous injection, beginning at 7 weeks and through euthanasia at 18 weeks. This dose of Cl-amidine has been published previously.^{26 (link),27 (link)} Mice were fed high-fat chow (42% from fat) beginning at 8 weeks and until euthanasia. For in vitro experiments, Cl-amidine was used at a concentration of 200 μmol/L.

Knight J.S., Luo W., O’Dell A.A., Yalavarthi S., Zhao W., Subramanian V., Guo C., Grenn R.C., Thompson P.R., Eitzman D.T, & Kaplan M.J. (2014). Peptidylarginine Deiminase Inhibition Reduces Vascular Damage and Modulates Innate Immune Responses in Murine Models of Atherosclerosis. Circulation research, 114(6), 947-956.

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Mouse Breeding and Housing for Research

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Wild type C57BL/6J (#000664),
Apoe^−/−(B6.129P2-Apoe^tm1Unc/J,
#002052), Tet2^−/−(B6(Cg)-Tet2^tm1.2Rao/J,
#023359), Ldlr^−/−(B6.129S7-Ldlr^tm1Her/J,
#002207), and CD45.1 mice
(B6.SJL-Ptprc^aPepc^b/BoyJ, #002014) were
purchased from The Jackson Laboratory (Bar Harbor, ME, USA). For all
experiments, littermates of the same sex were randomly assigned to
experimental groups. Mice were group-housed on a 12:12hrs light:dark cycle
at 22°C with access to standard mouse chow or diet and water
ad libitum. The study protocols were approved and
reviewed by the Institutional Animal Care and Use Committee (IACUC) at
Massachusetts General Hospital (Boston, MA, USA) and all animal experiments
were performed in compliance with relevant regulatory standards.

Heyde A., Rohde D., McAlpine C.S., Zhang S., Hoyer F.F., Gerold J.M., Cheek D., Iwamoto Y., Schloss M.J., Vandoorne K., Iborra-Egea O., Muñoz-Guijosa C., Bayes-Genis A., Reiter J.G., Craig M., Swirski F.K., Nahrendorf M., Nowak M.A, & Naxerova K. (2021). Increased stem cell proliferation in atherosclerosis accelerates clonal hematopoiesis. Cell, 184(5), 1348-1361.e22.

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Atherosclerosis Induction in ApoE-/- Mice

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Female C57BL/6J mice (wild type), female ubiquitous GFP mice [C57BL/6-Tg (UBC-GFP) 30Scha/J], and female apolipoprotein E–deficient mice (ApoE^−/−; B6.129P2-Apoetm1Unc/J) were purchased from The Jackson Laboratory. At 12 weeks of age, ApoE^−/− mice were fed an HCD (21.2% fat by weight and 0.2% cholesterol; TD.88137, Harlan Teklad) for 3 to 6 weeks. All procedures were approved by the Institutional Animal Care and Use Committee (IACUC) Subcommittee on Research Animal Care, Massachusetts General Hospital (MGH), Charlestown, MA.

Sager H.B., Dutta P., Dahlman J.E., Hulsmans M., Courties G., Sun Y., Heidt T., Vinegoni C., Borodovsky A., Fitzgerald K., Wojtkiewicz G.R., Iwamoto Y., Tricot B., Khan O.F., Kauffman K.J., Xing Y., Shaw T.E., Libby P., Langer R., Weissleder R., Swirski F.K., Anderson D.G, & Nahrendorf M. (2016). RNAi targeting multiple cell adhesion molecules reduces immune cell recruitment and vascular inflammation after myocardial infarction. Science translational medicine, 8(342), 342ra80.

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Atherosclerosis in ApoE-/- Mouse Model

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C57BL/6J and ApoE^-/- (B6.129P2-Apoe^tm1Unc/J) mice were purchased from The Jackson Laboratory. ApoE^-/- Aid^-/- double-knockout mice were generated in our mouse colony. Male mice were raised on chow diet until they reached full adult maturity at 12 weeks of age and switched to high-fat diet (#D12079B, Research Diets Inc., 21% fat and 0.15% cholesterol) until 28 weeks of age to exacerbate plaque formation. Only male mice were used to eliminate any effects of sex on disease severity (28 (link)). Cholesterol levels were measured from animals that fasted overnight using an HDL and LDL/VLDL Quantitation Kit (Sigma) per manufacturer’s recommendations. All animal protocols were reviewed and approved by the Animal Care and Use Committee of the National Institute on Aging.

Hutchinson M.A., Park H.S., Zanotti K.J., Alvarez-Gonzalez J., Zhang J., Zhang L., Telljohann R., Wang M., Lakatta E.G., Gearhart P.J, & Maul R.W. (2021). Auto-Antibody Production During Experimental Atherosclerosis in ApoE-/- Mice. Frontiers in Immunology, 12, 695220.

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Atherosclerosis induction in CXCR4-deficient mice

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Mice were housed in specific pathogen-free animal facilities, maintained by Washington University School of Medicine. Apoe^−/− (B6.129P2-Apoe^tm1Unc/J, 002052) mice were purchased from Jackson Laboratories. Diet was switched to high fat diet (HFD) (Teklad, TD.88137) containing 21% milk fat and 0.15% cholesterol from 5–6 weeks of age for 10 weeks to accelerate atherosclerotic plaque formation. Tamoxifen-inducible endothelial specific CXCR4 deficient mice were generated by crossing Cxcr4^flox/flox (B6.129P2-Cxcr4^tm2Yzo/J, 008767) mice purchased from Jackson Laboratories with VE-cadherin-CreERT2 (C57BL/6-Tg(Cdh5-cre/ERT2)1^Rha) mice^{22 (link)}. To induce atherosclerosis formation, they were injected with 5.0 × 10¹¹ genome copies (GC) of adeno-associated virus 2 vector encoding murine PCSK9 (AAV-mPCSK9 vector, Vector Biolabs) intravenously at 5–6 weeks old, and fed with HFD for 10 weeks. Activation of cre recombinase was induced by oral administration of tamoxifen every 3 days over a 9-day period, 1 week before the PET imaging analysis. All experiment procedures were performed in compliance with guidelines set forth by the NIH Office of Laboratory Animal Welfare and approved by the Institutional Animal Care and Use Committee of Washington University.

Baba O., Huang L.H., Elvington A., Szpakowska M., Sultan D., Heo G.S., Zhang X., Luehmann H., Detering L., Chevigné A., Liu Y, & Randolph G.J. (2020). CXCR4-binding PET tracers link monocyte recruitment and endothelial injury in murine atherosclerosis. Arteriosclerosis, thrombosis, and vascular biology, 41(2), 822-836.

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Generating Hypercholesterolemic RBC-Arg1 Knockout Mice

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To generate hypercholesterolemic mice lacking ARG1 specifically in red blood cells (RBCs), transgenic mice expressing an improved GFPcre fusion protein controlled by the endogenous erythropoietin receptor (EpoR) promoter (ErCre) 21 (link) were first backcrossed into the C57BL6/J (Janvier) background (for > 8 generations; not shown) before being crossed with apolipoprotein E-deficient mice (apoE -/-; B6.129P2-Apoe tm1Unc /J; The Jackson Laboratory; Stock No. 002052). EpoR is predominantly expressed on cells of the erythroid lineage. [22] (link)[23] [24] [25] Male ErCre transgenic (tg) apoE -/-mice were then crossed with female floxed mutant mice possessing loxP sites flanking exons 7 and 8 of the Arg1 gene (ARG1 flox ; The Jackson Laboratory; Stock No. 008817). Male and female ErCre transgenic (apoE -/-RBC. ARG1-knockout) and wild-type (apoE -/-RBC.ARG1-wild-type [WT]) apoE -/-ARG1 flox/flox littermates were used and examined separately throughout the study. All mice were fed modified Western type diet containing 1.25% cholesterol and 16 mg/ kg folic acid (TD88137; ssniff-Spezialdiäten GmbH) beginning at the age of 5 weeks for a total of 15 or 20 weeks. These time points were chosen based on previous histological time

Gogiraju R., Renner L., Bochenek M.L., Zifkos K., Molitor M., Danckwardt S., Wenzel P., Münzel T., Konstantinides S, & Schäfer K. (2022). Arginase-1 Deletion in Erythrocytes Promotes Vascular Calcification via Enhanced GSNOR (S-Nitrosoglutathione Reductase) Expression and NO Signaling in Smooth Muscle Cells. Arteriosclerosis, thrombosis, and vascular biology, 42(12).

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Genetic Knockout Mouse Models

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C57Bl/6J (WT), B6.SJL-PtprcaPepcb/BoyJ (CD45.1⁺), B6.129P2(SJL)-Myd88tm1.1Defr/J (Myd88^−/−), B10.129S2(B6)-Ighmtm1Cgn/J (µMT), B6.Cg-Tg(TcraTcrb)425Cbn/J (OT-II), B6.129S7-Ldlrtm1Her/J (Ldlr^−/−) and B6.129P2-Apoetm1Unc/J (Apoe^−/−) were purchased from The Jackson Laboratory (Bar Harbor, ME). GM-CSF-deficient mice (Csf2^−/−) were kindly provided by Dr. Randy Seeley, University of Cincinnati, USA. GM-CSF-receptor deficient mice (Csf2rb^−/−) were kindly provided by Dr. Jeffrey Whitsett, Cincinnati Children’s Hospital Medical Center, USA. All protocols are approved by the Animal Review Committee at Massachusetts General Hospital.

Hilgendorf I., Theurl I., Gerhardt L.M., Robbins C.S., Weber G.F., Gonen A., Iwamoto Y., Degousee N., Holderried T.A., Winter C., Zirlik A., Lin H.Y., Sukhova G.K., Butany J., Rubin B.B., Witztum J.L., Libby P., Nahrendorf M., Weissleder R, & Swirski F.K. (2014). Innate Response Activator B Cells Aggravate Atherosclerosis by Stimulating TH1 Adaptive Immunity. Circulation, 129(16), 1677-1687.

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