Inos b6.129p2 nos2tm1lau j

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The INOS−/− (B6.129P2-Nos2tm1Lau/J) is a genetically modified mouse strain that lacks the iNOS (inducible nitric oxide synthase) gene. This strain is commonly used in research to study the role of nitric oxide in various biological processes.

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8 protocols using inos b6.129p2 nos2tm1lau j

Mouse Breeding and Maintenance Protocols

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Two to four month old male and female mice, bred and maintained at Rider University, were handled in accord with NIH, Animal Welfare Act, and Rider University IACUC guidelines. Breeding pairs of C57BL/6J, BALB/c, CB17-Prkdc^scid/J, IFNγR^−/− (B6.129S7^Ifngr/J), iNOS^−/− (B6.129P2-Nos2^tm1Lau/J), and IL4^−/− (B6.129P2-IL4^tm1Cgn/J) mice were obtained from the Jackson Laboratory, Bar Harbor, ME.

Goldman N., Valiuskyte K., Londregan J., Swider A., Somerville J, & Riggs J.E. (2017). Macrophage regulation of B cell proliferation. Cellular immunology, 314, 54-62.

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Genetically Modified Murine Models

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C57BL/6 mice were purchased from the National Cancer Institute (Fredericksburg, MD). CCR2-/- (B6.129S4-Ccr2^tm1Ifc/J), Phox-/- (B6.129S-Cybb^tm1Din/J), iNOS-/- (B6.129P2-Nos2^tm1Lau/J), and RAG-/- (B6.129S7-Rag1^tm1Mom/J) mice were purchased from The Jackson Laboratory. All mice were maintained in a specific pathogen-free environment at the University of Pennsylvania Animal Care Facility.

Glennie N.D., Volk S.W, & Scott P. (2017). Skin-resident CD4+ T cells protect against Leishmania major by recruiting and activating inflammatory monocytes. PLoS Pathogens, 13(4), e1006349.

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Breeding and Handling of Mouse Strains

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Two to four month old male and female mice, bred and maintained at Rider University, were handled in accord with NIH, Animal Welfare Act, and Rider University IACUC guidelines. Breeding pairs of C57BL/6J, BALB/c, IFNγR^−/− (B6.129S7^Ifngr/J), and iNOS^−/− (B6.129P2-Nos2^tm1Lau/J) mice were obtained from the Jackson Laboratory, Bar Harbor, ME.

Wood M.A., Goldman N., DePierri K., Somerville J, & Riggs J.E. (2016). Erythropoietin increases macrophage-mediated T cell suppression. Cellular immunology, 306-307, 17-24.

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Investigating iNOS deficiency in mice

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Wild-type C57BL/6 and iNOS^−/− (B6.129P2-Nos2^tm1Lau/J) mice were obtained from The Jackson Laboratory (Bar Harbor, ME). Mice were maintained and bred in the Experimental Animal Facility of the National Centre for Cell Science (NCCS), Pune, India. All mice experiments were performed with the protocols approved by the Institutional Animal Ethics Committee. (Project Id: EAF/2016/B-257).

Sonar S.A, & Lal G. (2019). The iNOS Activity During an Immune Response Controls the CNS Pathology in Experimental Autoimmune Encephalomyelitis. Frontiers in Immunology, 10, 710.

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Rodent Models for Neuroimmune Research

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Young (3-4 months) and middle-aged (10-12 months) female Sprague-Dawley rats were obtained from Harlan Inc. (Indianapolis, IN) . Breeding pairs of young (6-8 weeks old) female and male WT (C57BL/10J; Stock No. 000664) and interleukin-1 receptor KO (IL-1R-/-: B6.129S7-Illr1 tm1Imx /J; Stock No. 003245) and inducible nitric oxide synthase (iNOS) KO (iNOS-/-: B6.129P2-Nos2 tm1Lau /J; Stock No. 002609) mice were purchased from Jackson Laboratories. Housing was light-controlled (lights on from 07:00 to 19:00 h) and airconditioned (23 ± 2°C) and the animals were fed chow and water ad libitum. Mice were bred and female offspring were genotyped and used in the study when they were 3-4 months old.

Gilbreath E.T., Jaganathan L., Subramanian M., Balasubramanian P., Linning K.D., MohanKumar S.M.J, & MohanKumar P.S. (2019). Chronic estrogen affects TIDA neurons through IL-1β and NO: effects of aging. The Journal of endocrinology, 240(2).

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Myeloid-Specific HIF-1α and iNOS Knockout Mice

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Wildtype mice were C57BL/6, were obtained from Jackson Laboratory, and then bred in house. All knockout mice are on the C57BL/6 background. B6.129-Hif1a^tm3Rsjo/J (HIF1α^flox) mice were obtained from the Jackson Laboratory and were crossed with B6.129P2-Lyz2^tm1(cre)Ifo/J (LysMcre) to generate Hif1a^flox/flox, LysMcre^+/+ mice that had Hif1a deletion targeted to the myeloid lineage. B6.129P2-Nos2^tm1Lau/J (iNOS-) mice were obtained from the Jackson Laboratory and were bred in house, and also crossed to Hif1a^flox/flox, LysMcre^+/+ mice to generate Hif1a^flox/flox, LysMcre^+/+, Nos2^−/− mice. NFkB-RE-luc mice (10499, Taconic) on the BALB/c background were obtained and BMDM were prepared from these mice for NFkB-luciferase experiments.

Braverman J, & Stanley S.A. (2017). Nitric oxide modulates macrophage responses to M. tuberculosis infection through activation of HIF-1α and repression of NF-kB. Journal of immunology (Baltimore, Md. : 1950), 199(5), 1805-1816.

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Inflammatory Response in Murine Models

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In our experiments we employed female C57BL/6 J wild-type (WT) and B6.129P2-Nos2tm1Lau/J (iNOS^−/−) 6–8-week-old mice purchased from The Jackson Laboratory (Bar Harbor, ME, USA). Animal studies were approved by the Animal Care and Use Committee of the University of Louisville (Louisville, KY, USA).

Adamiak M., Abdelbaset-Ismail A., Moore JB I.V., Zhao J., Abdel-Latif A., Wysoczynski M, & Ratajczak M.Z. (2016). Inducible Nitric Oxide Synthase (iNOS) Is a Novel Negative Regulator of Hematopoietic Stem/Progenitor Cell Trafficking. Stem Cell Reviews, 13(1), 92-103.

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Genetic mouse models for in vivo research

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Breeding pairs of C57BL/6J, B6.129S-Cybb^tm1Din/J (gp91^phox-/-), B6.129X1-Mpo^tm1Lus/J (MPO^-/-) and B6.129P2-Nos2^tm1Lau/J (iNOS^-/-) mice were purchased from Jackson Laboratory (Bar Harbor, USA). We used 8- to 12-week-old female mice for our in vivo experiments, and these animals were all bred and raised under the same conditions in the central animal housing facility of the University of Tübingen. B6(Cg)-Padi4^tm1.2Kmow/J mice (PAD4^-/-) were kindly provided by Prof. Wolfram Ruf, University of Mainz. All the experimental protocols were approved by Regierungspräsidium Tübingen.

Mehling R., Schwenck J., Lemberg C., Trautwein C., Zizmare L., Kramer D., Müller A., Fehrenbacher B., Gonzalez-Menendez I., Quintanilla-Martinez L., Schröder K., Brandes R.P., Schaller M., Ruf W., Eichner M., Ghoreschi K., Röcken M., Pichler B.J, & Kneilling M. (2021). Immunomodulatory role of reactive oxygen species and nitrogen species during T cell-driven neutrophil-enriched acute and chronic cutaneous delayed-type hypersensitivity reactions. Theranostics, 11(2), 470-490.

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