b6 cmv-cre transgenic mice  (Jackson Laboratory)

Journal: Scientific Reports

Article Title: Viral-mediated fusion of mesenchymal stem cells with cells of the infarcted heart hinders healing via decreased vascularization and immune modulation

doi: 10.1038/srep20283

Figure Lengend Snippet: Detection and augmentation of MSC cell fusion in vivo ( a ) Schematic of the in vivo Cre/ LoxP biophotonic detection system. MSCs are transfected with a LoxP -stop codon- LoxP -luciferase plasmid prior to cell transplantation. The MSCs are transplanted into mice, which constitutively express Cre recombinase. Upon fusion between MSCs and a cell of the Cre mouse, Cre recombinase excises the LoxP -stop codon- LoxP sequence and luciferase is expressed in the fusion product. The fusion product can then emit a bioluminescent signal after the addition of a luciferin substrate. ( b ) Quantification of the day 7 mean luminescent signal (photons/centimeters 2 /second/steradian, photons/cm 2 /s/sr) for each treatment group (sham, MSC, and MSC-VSVG). The MSC and MSC-VSVG emitted a significantly higher mean luminescent signal compared to the sham control group (* P < 0.05, data is displayed as average (Avg) + standard deviation (SD)). Three representative luminescent overlay images for each group are shown below graph.

Article Snippet: We used transgenic mice that constitutively express Cre recombinase (B6.C-Tg[CMV-cre]1Cgn/J; Jackson Laboratory, Bar Harbor, ME) (15 total mice, 5 per treatment group, 2 months old), such that deletion of LoxP -flanked genes occurs in all tissues, including germ cells.

Techniques: In Vivo, Transfection, Luciferase, Plasmid Preparation, Transplantation Assay, Sequencing, Control, Standard Deviation

Journal: Blood

Article Title: The mouse NKR-P1B:Clr-b recognition system is a negative regulator of innate immune responses

doi: 10.1182/blood-2014-02-556142

Figure Lengend Snippet: NKR-P1B-deficient mice show impaired acute rejection of Clr-b-deficient splenocytes but enhanced rejection of MHC-I-deficient splenocytes. (A) Rejection of 5-(and 6)-carboxyfluorescein diacetate succinimidyl ester (CFSE)-labeled splenocytes from Clr-b−/− mice 18 hours after injection. Some mice were treated with poly(I:C) or CpG-B ODN for 24 or 6 hours, respectively, before CFSE-labeled splenocyte injection. Each symbol represents an individual mouse. Small horizontal bars represent mean values. Data are pooled from multiple experiments. (B) Rejection of CFSE-labeled splenocytes from Clr-b−/− mice 18 hours after injection. Some of the WT mice were treated with anti-NKR-P1C antibody (NK1.1) to deplete NK cells (NK-depleted). All mice were treated with CpG-B ODN for 6 hours before CFSE-labeled splenocyte injection. Each symbol represents an individual mouse. Small horizontal bars represent mean values. Data are pooled from 2 independent experiments. (C) Rejection of CFSE-labeled splenocytes from B2m−/− and B2m−/−Clr-b−/− mice at different time points after injection. Mice were not stimulated before splenocyte injection. Mean ± SD of percent rejection at each time point is shown. Data are pooled from multiple experiments. Statistical analysis was performed by Student t test, and P values are indicated. (D) Ability of LAK cells from WT and NKR-P1B-deficient mice to mediate cytotoxicity toward B2m−/− or B2m−/−Clr-b−/− BM-DCs was tested by 51Cr-release assay. Data are represented as the mean ± SD of percent killing measured in triplicate. Statistical analysis was performed by Student t test, and P values are indicated.

Article Snippet: Mice C57BL/6 (B6), β 2 m-deficient ( B2m −/− ) (B6.129P2- B2m tm1Unc /J), CMV-cre transgenic (Tg) (B6.C-Tg[CMV-cre]1Cgn/J), and Eμ-myc Tg (B6.Cg-Tg[IghMyc]22Bri/J) mice were purchased from The Jackson Laboratory (Bar Harbor, ME).

Techniques: Labeling, Injection, Release Assay