Genetically Modified Mouse Strains for Cell Lineage Tracking

C57BL/6J (wild type, WT), B6.SJL-Ptprc^aPepc^b/BoyJ (CD45.1⁺), C57BL/6-Tg(UBC-GFP)30Scha/J (GFP⁺), B6.129X1-Nfe2l2^tm1Ywk/J (Nrf2^−/−), B6.Cg-Msr1^tm1Csk/J (Msr1^−/−), B6.129S1-Cd36^tm1Mfe/J (CD36^−/−), B6.129-Hba^tm1(HBA)Tow/Hbb^{tm2(HBG1,HBB*)Tow} (sickle cell disease, SCD) and B6.129-Hba^tm1(HBA)Tow/Hbb^{tm3(HBG1,HBB*)Tow} (non-sickling transgenic control, tgCtrl.) mice were purchased from The Jackson Laboratory (Bar Harbor, ME, USA). GM-CSF-deficient mice (Csf2^−/−) on a C57BL/6J background were bred in-house. B6.129S6-Gt(ROSA)26Sor^{tm9(CAG-tdTomato)Hze}/J (ROSA26-tdTomato^fl/fl or R26-tdT) and B6.129P2(Cg)-B6.129P2(C)-Cx3cr1^{tm2.1(cre/ERT2)Jung}/J (Cx3cr1-CreERT2) ^{24 (link),25 (link)} were kindly provided by Prof. Dr. M. Prinz. Mice carrying the myeloid-specific knockout of the FPN1 gene (LysM^Cre/+ Slc40a1^fl/fl) were kindly provided by Dr. F. Wang, back-crossed on a C57BL/6 background and bred in house. Unless otherwise indicated age- and sex-matched animals were used at 8 – 12 weeks of age. Where appropriate, animals were randomly assigned to interventions. All protocols were approved by the Animal Review Committee at Massachusetts General Hospital (Protocol No. 2011N000035 and 2015N000044) and by the Federal Ministry of Science, Research and Economy in Austria (Project No. BMWFW-66.011/0115-WF/V/3b/2014).

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Theurl I., Hilgendorf I., Nairz M., Tymoszuk P., Haschka D., Asshoff M., He S., Gerhardt L.M., Holderried T.A., Seifert M., Sopper S., Fenn A.M., Anzai A., Rattik S., McAlpine C., Theurl M., Wieghofer P., Iwamoto Y., Weber G.F., Harder N.K., Chousterman B.G., Arvedson T.L., McKee M., Wang F., Lutz O.M., Rezoagli E., Babitt J.L., Berra L., Prinz M., Nahrendorf M., Weiss G., Weissleder R., Lin H.Y, & Swirski F.K. (2016). On-demand erythrocyte disposal and iron recycling requires transient macrophages in the liver. Nature medicine, 22(8), 945-951.

Publication 2016

B6.129X1-Nfe2l2tm1Ywk/J

Animal Csf2 Ert2 Gm csf Knockout gene Mice Nrf2 Rosa Sickle cell disease Tdtomato Transgenic

Corresponding Organization :

Other organizations : Center for Systems Biology, Harvard University, Massachusetts General Hospital, Innsbruck Medical University, Universität Innsbruck, University Hospital Bonn, University Medical Center Freiburg, Amgen (United States), Zhejiang University, Austrian Drug Screening Institute (Austria)

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Variable analysis

independent variables

Genotype of mice (C57BL/6J (wild type, WT), B6.SJL-Ptprc^a Pepc^b/BoyJ (CD45.1+), C57BL/6-Tg(UBC-GFP)30Scha/J (GFP+), B6.129X1-Nfe2l2^tm1Ywk/J (Nrf2−/−), B6.Cg-Msr1^tm1Csk/J (Msr1−/−), B6.129S1-Cd36^tm1Mfe/J (CD36−/−), B6.129-Hba^tm1(HBA)Tow/Hbb^tm2(HBG1,HBB*)Tow (sickle cell disease, SCD), B6.129-Hba^tm1(HBA)Tow/Hbb^tm3(HBG1,HBB*)Tow (non-sickling transgenic control, tgCtrl.), GM-CSF-deficient mice (Csf2−/−))
Myeloid-specific knockout of the FPN1 gene (LysM^Cre/+ Slc40a1^fl/fl)

dependent variables

Not explicitly mentioned

control variables

Age- and sex-matched animals used at 8 – 12 weeks of age
Where appropriate, animals were randomly assigned to interventions

positive controls

C57BL/6J (wild type, WT)
B6.129-Hba^tm1(HBA)Tow/Hbb^tm3(HBG1,HBB*)Tow (non-sickling transgenic control, tgCtrl.)

negative controls

B6.129-Hba^tm1(HBA)Tow/Hbb^tm2(HBG1,HBB*)Tow (sickle cell disease, SCD)

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