Hepatocyte-specific SOCS1-deficient mice, generated by crossing Socs1fl/fl mice with albumin-Cre (AlbCre) mice, have been already described [15 (link)]. Socs3fl/fl mice were purchased from the Jackson laboratories (B6;129S4-Socs3tm1Ayos/J) and hepatocyte-specific SOCS3-deficient mice were generated by crossing them with AlbCre mice. All animal experiments were carried out with the approval of the Université de Sherbrooke Ethical committee on animal experimentation (protocol number 226-17B) under the guidelines set by the Canadian Council on Animal care (CCAC). Partial hepatectomy was carried out on 8–10 weeks old mice under isoflurane anesthesia (2% isoflurane mixed with oxygen) as detailed previously [26 (link)], and remnant liver tissues were harvested after 24 h. Experimental HCC was induced by the administration of diethyl nitrosamine (DEN) to 2-weeks old male pups as previously described [15 (link)]. The mice were euthanized after 8 months and macroscopic liver tumor nodules and adjacent normal tissues were resected. Euthanasia was carried out using CO2 at a 25% flow rate under isoflurane anaesthesia. Small pieces of tissues were immersed in RNAlater (ThermoFisher) and stored at -20 °C for gene expression analysis.
B6 129s4 socs3tm1ayos j
Manufactured by Jackson ImmunoResearch
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B6;129S4-Socs3tm1Ayos/J is a genetically modified mouse strain. It has a targeted mutation in the Socs3 gene, which is involved in the regulation of cytokine signaling pathways.
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Lab products found in correlation
Redextract n amp tissue pcr kit, by Merck Group (2 mentions)
Rnalater, by Thermo Fisher Scientific (1 mentions)
C57bl 6j mice, by Jackson ImmunoResearch (1 mentions)
B6.129 leprtm2 cre rck j, by Jackson ImmunoResearch (1 mentions)
B6 129s6 gt rosa 26sortm9 cag tdtomato hze j, by Jackson ImmunoResearch (1 mentions)
Tg nr5a1 cre 7lowl j, by Jackson ImmunoResearch (1 mentions)
4 protocols using b6 129s4 socs3tm1ayos j
1
Hepatocyte-specific SOCS1/SOCS3 Knockout Mice
2
Endothelial SOCS3-Knockout Mouse Model
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Endothelial specific, tamoxifen-inducible SOCS3-knockout mice were generated by breeding B6.Tg(Cdh5-cre/ERT2)1Rha (Cdh5-CreERT2 endothelial driver) mice (91 (link)) (a gift from Kevin Pumiglia, Albany Medical College, Albany, New York, USA) with B6.Gt(ROSA)26Sortm9(CAG-tdTomato)Hze (ROSA26-tdTomato reporter) (92 (link)) and B6;129S4-Socs3tm1Ayos/J (SOCS3fl/fl conditional knockout) (93 (link)) mice (The Jackson Laboratory). Mice were backcrossed to a full C57BL6/J background by breeding to C57BL6/J mice (The Jackson Laboratory) for at least 10 generations. Knockouts and heterozygous and control littermates were obtained by crossing Cre+ tdTomato+ SOCS3fl/+ mice. Genotypes and sex were confirmed by PCR genotyping (Supplemental Table 4 ). All mice received tamoxifen (2 mg tamoxifen in 100 μL via intraperitoneal [IP] injection) at 6–9 weeks old for 5 consecutive days. Deletion of the target gene after tamoxifen was confirmed by tail digestion and PCR. All the experiments were conducted between 2 and 3 weeks after the end of tamoxifen treatment.
3
Conditional Deletion of Socs3 in LepR-Expressing Cells
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The deletion of Socs3 gene in LepR‐expressing cells was achieved by breeding the LepR‐IRES‐Cre strain (B6.129‐Leprtm2(cre)Rck/J, Jackson Laboratories) with the SOCS3‐floxed mouse (B6;129S4‐SOCS3tm1Ayos/J, Jackson Laboratories), as previously described and validated (Pedroso et al. 2014 , 2016 ; Zampieri et al. 2015 , 2016 ; Bohlen et al. 2016 ). Animals carrying the SOCS3 conditional deletion in LepR‐expressing cells (SOCS3 KO group) were homozygous for the loxP‐flanked Socs3 and LepR‐Cre alleles. The control group was composed of littermate animals carrying only the LepR‐Cre allele in homozygosity. Control and SOCS3 KO mice were weaned at 3–4 weeks of age and their mutations were confirmed by genotyping the DNA that had been previously extracted from the tail tip (REDExtract‐N‐Amp™ Tissue PCR Kit, Sigma). Mice were maintained under standard conditions of light (12‐h light/dark cycle) and temperature (23 ± 1°C). All animal procedures were approved by the Ethics Committee on the Use of Animals of the Institute of Biomedical Sciences at the University of São Paulo, and were performed according to the ethical guidelines adopted by the Brazilian College of Animal Experimentation.
4
SF1-Specific SOCS3 Inactivation in Mice
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Mice expressing the Cre recombinase under SF1 promoters (Tg(Nr5a1-cre)7Lowl/J, The Jackson Laboratory, Bar Harbor, ME, USA) were bred with animals carrying a loxP-flanked Socs3 allele (B6.129S4-Socs3tm1Ayos/J, The Jackson Laboratory). Mice carrying an SF1-specific SOCS3 inactivation (SF1 Socs3 KO group) were homozygous for the loxP-flanked Socs3 allele and carried the Cre transgene, whereas the control group was composed of littermate mice carrying only the loxP-flanked Socs3 allele 235:3 in homozygosity. SF1-Cre animals were also bred with the Cre-inducible tdTomato-reporter mouse (B6;129S6-Gt(ROSA)26Sortm9(CAG-tdTomato)Hze/J, The Jackson Laboratory). The purpose of this breeding was to allow the visualization of SF1-positive cells through the red fluorescent tdTomato protein. Mice were weaned at 3-4 weeks of age and genotyped through PCR using DNA extracted from the tail tip (REDExtract-N-Amp Tissue PCR Kit, Sigma-Aldrich). Mice were bred and maintained under standard conditions of light (12-h light/darkness cycle; lights on at 8:00 h) and temperature (22 ± 2°C). In all experiments, animals received a regular rodent chow diet (2.99 kcal/g; 9.4% calories from fat; Quimtia, Colombo, Brazil). The animal procedures were approved by the Ethics Committee on the Use of Animals of the Institute of Biomedical Sciences at the University of São Paulo (protocol number 71/2016).
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