B6 cg ccl2tm1.1pame j

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The B6.Cg-Ccl2tm1.1Pame/J is a mouse strain that contains a targeted mutation in the Ccl2 gene. The Ccl2 gene encodes the chemokine (C-C motif) ligand 2, which is involved in the recruitment of monocytes, memory T cells, and dendritic cells. This mouse strain can be used to study the role of Ccl2 in various biological processes.

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5 protocols using b6 cg ccl2tm1.1pame j

Conditional Knockout of Mcp-1 in Podocytes

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IACUC protocol approval was obtained at the University of Pittsburgh. Control littermates and Podo-Mcp-1^fl/fl mice were afforded the ethical and scientific standards recommended by the Guide for the Care and Use of Laboratory Animals of the National Institutes of Health. ARRIVE guidelines were followed [54 (link)]. Male 8- to 12-week-old mice were housed (maximum 4 males/cage) in plastic cages with wood chips in the animal facility at 72 °C and 39.6% humidity on a 12:12 h light–dark cycle with water and Prolab^® IsoPro^® RMH 3000 5P75 diet (PMI Nutrition International, LLC, Arden Hills, MN, USA) provided ad libitum.
To generate Cre-lox conditional knockout (Podo-Mcp-1^fl/fl) mice, female B6.Cg-Ccl2^tm1.1Pame/J containing the loxP sites flanking exons 2 and 3 of the C-C motif ligand 2 (Ccl2/Mcp-1) (#016849, Jackson Laboratory, Bar Harbor, ME) [55 (link)] were crossed with male B6.Cg-Tg(NPHS2-Cre)295Lbh/J expressing Cre recombinase under the control of the podocin (NPHS2) promoter (#008205, Jackson Laboratory) [56 (link)]. All mice are on a C57BL/6J background.

Bondi C.D., Hartman H.L., Rush B.M, & Tan R.J. (2024). Podocyte-Specific Deletion of MCP-1 Fails to Protect against Angiotensin II- or Adriamycin-Induced Glomerular Disease. International Journal of Molecular Sciences, 25(9), 4987.

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Murine Models for Immunological Studies

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C57BL/6 (WT), B6.SJL-Ptprc^aPepc^b/BoyJ, C57BL/6-Tg(UBC-GFP)30Scha/J (GFP⁺), B6.129P2(SJL)-Myd88^tm1.1Defr/J, B6.129-Tlr2^tm1Kir/J, B6(Cg)-Tlr4^tm1.2Karp/J, B6.129S1-Tlr7^tm1Flv/J, C57BL/6J-Tlr9^M7Btlr/Mmjax, B6.129S7-Il1r1^tm1/mx/J, C57BL/6J-Ticam1^Lps2/J, B6.Cg-Ccl2^tm1.1Pame/J, and B6.129S4-Ccr2^tm1lfc/J (The Jackson Laboratory) were used in this study. Csf2^−/− and Csf2rb^−/− mice on C57BL/6 background (10 generations) were bred in-house (Rauch et al., 2012 (link); Hilgendorf et al., 2014b (link); Weber et al., 2014 (link)). All experiments were conducted with male mice aged 8–16 wk at the time of death. All protocols were approved by the Animal Review Committee at Massachusetts General Hospital.

Anzai A., Choi J.L., He S., Fenn A.M., Nairz M., Rattik S., McAlpine C.S., Mindur J.E., Chan C.T., Iwamoto Y., Tricot B., Wojtkiewicz G.R., Weissleder R., Libby P., Nahrendorf M., Stone J.R., Becher B, & Swirski F.K. (2017). The infarcted myocardium solicits GM-CSF for the detrimental oversupply of inflammatory leukocytes. The Journal of Experimental Medicine, 214(11), 3293-3310.

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Conditional Knockout of Lkb1 in Kidney

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All animal experiments were conducted according to the guidelines of the National Institutes of Health Guide for the Care and Use of Laboratory Animals, as well as the German law for the welfare of animals, and were approved by regional authorities (Regierungsprasidium Freiburg, 35-9185.81/G-16/27). Mice were housed in a specific pathogen-free facility, fed ad libitum and housed at constant ambient temperature in a 12-hour day/night cycle. Breeding and genotyping were done according to standard procedures.
Lkb1 flox/flox mice (mixed genetic background) and Ccl2-RFP flox/flox (B6.Cg-Ccl2tm1.1Pame/J, stock number : 016849, C57BL/6 genetic background) were purchased from The Jackson Laboratories (STOCK Stk11 tm1.1Sjm /J, stock number: 014143) and were crossed to KspCre mice (B6.Cg-Tg(Cdh16-cre)91lgr/J; C57Bl/6N background) 22 Experiments were conducted on both females and males.

Quatredeniers M., Bienaimé F., Ferri G., Isnard P., Porée E., Billot K., Birgy É., Ceccarelli S., Silbermann F., Braeg S., Nguyen‐Khoa T., Salomon R., Corvol P., Kuehn E.W., Saunier S., & Burtin M. (2021). The renal inflammatory network of nephronophthisis.

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Conditional Knockout of Lkb1 in Kidney

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Quatredeniers M., Bienaimé F., Ferri G., Isnard P., Porée E., Billot K., Birgy E., Mazloum M., Ceccarelli S., Silbermann F., Braeg S., Nguyen-Khoa T., Salomon R., Gubler M.C., Kuehn E.W., Saunier S, & Viau A. (2022). The renal inflammatory network of nephronophthisis. Human molecular genetics, 31(13).

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Murine Models for Neuroinflammation Studies

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All experiments were conducted in accordance with national guidelines for the use of experimental animals, and all protocols were approved by the German governmental committees (Regierung von Oberbayern, Munich, Germany). 83 wild-type male C57BL6/J mice were obtained from Charles River. 17 Rag1 -/-(B6.129S7-Rag1 tm1Mom/J ), 10 CAG-EGFP (C57BL/6-Tg (CAG-EGFP)131 osb/LeySopJ ), 22 heterozygous PA-UBC-GFP (B6.Cg-Ptprc Tg (UBC-PA-GFP)1 Mnz/J ), 5 CCL2-RFP (B6.Cg-Ccl2tm1.1 Pame/J ) and 5 CCL2 -/-(B6.129S4-Ccl2tm1 Rol/J ) male mice were obtained from Jackson Laboratories (USA). Eight female LysM-eGFP (Lyz2tm1.1 Graf ) mice were kindly donated by M.Sperandio (Walter BrendlCenter for Experimental Research, Munich, Germany). CCR2 RFP/RFP CX3CR1 GFP/+ and CCR2 RFP/+ CX3CR1 GFP/+ mice were originally generated by Israel Charo and Richard Ransohoff [32] (link) and bred at the Theodor Kocher Institute, University of Bern, Switzerland. All other animals were housed at the core animal facility of the Institute for Stroke and Dementia Research, Munich, under controlled temperature (22 ± 2 °C), with a 12-h light-dark cycle period and had access to pelleted food and water ad libitum. All animals used for this study were at 8-12 weeks of age, expect for the aged mice which were 8 months old. Number of excluded animals from each experiment is shown in Suppl. Table 1.

Llovera G., Benakis C., Enzmann G., Cai R., Arzberger T., Ghasemigharagoz A., Mao X., Malik R., Lazarevic I., Liebscher S., Ertürk A., Meissner L., Vivien D., Haffner C., Plesnila N., Montaner J., Engelhardt B, & Liesz A. (2017). The choroid plexus is a key cerebral invasion route for T cells after stroke. Acta neuropathologica, 134(6).

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