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B6 cg spp1tm1blh j

Manufactured by Jackson ImmunoResearch
Sourced in United States

B6.Cg-Spp1tm1Blh/J is a genetically modified mouse strain. This strain carries a targeted mutation in the Spp1 gene, also known as osteopontin. The mutation results in the disruption of the Spp1 gene function.

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4 protocols using b6 cg spp1tm1blh j

1

Genetically Engineered Mice for Liver Research

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C57BL/6J wild-type (WT) and Opn−/− (B6.Cg-Spp1tm1Blh/J) mice were obtained from the Jackson Laboratory (Bar Harbor, Maine, USA). Opn+/− mice were intercrossed and littermates were used in all experiments. The Opn transgenic mice overexpressing OPN in hepatocytes (OpnHep Tg) under the serum amyloid-P component promoter were donated by Dr Mochida (Saitama Medical University, Saitama, Japan).10 (link) These mice were crossbred for 10 generations with the same strain and stock number of C57BL/6J WT listed above. The Hmgb1fl/fl mice were donated by Dr Billiar (University of Pittsburgh, Pittsburgh, Pennsylvania, USA). In these mice, the Hmgb1loxP allele was created by inserting loxP sites within introns 1 and 2 flanking exon 2 of Hmgb1.11 (link) The Hmgb1fl/fl mice were bred with Alb.Cre mice (the Jackson Laboratory) to generate hepatocyte-specific Hmgb1fl/flAlb.Cre mice (abbreviated as Hmgb1ΔHep). All animals received humane care according to the criteria outlined in the ‘Guide for the Care and Use of Laboratory Animals’ prepared by the National Academy of Sciences and published by the National Institutes of Health.
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2

OPN Knockout Mice Study

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All animal studies were approved by the Institutional Animal Care and Use Committees of Renji Hospital Clinical Stem Cell Research Center and Shanghai Jiao Tong University. OPN knockout (OPN-/-) mice (B6.Cg-Spp1tm1Blh/J) and their wild-type (WT) control C57BL/6J mice were purchased from the Jackson Laboratory (Bar Harbor, ME).
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3

Aging and OPN Knockout Mice Study

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Old (19–21 mos) and young (2–3 mos) BALB/c mice were purchased from Charles River Laboratories (Wilmington, MA) under a contractual arrangement with the National Institute on Aging. OPN-/- or knockout (OPN KO) were purchased from Jackson Laboratory (strain B6.Cg-Spp1tm1Blh/J) and were backcrossed with wildtype (WT) C57BL/6 that were also purchased from Jackson Laboratories. All animal work was approved by and performed in accordance with the policies of the University of South Florida Institutional Animal Use and Care Committee.
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4

Spp1 Deficiency Alters Silica-Induced Lung Inflammation

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Male and female Spp1+/+ (C57BL/6J), ovariectomized (OVX) Spp1+/+ (C57BL/6J) female, and Spp1–/– (B6.Cg-Spp1tm1Blh/J) (Liaw et al. 1998 (link)) mice were obtained from Jackson Laboratories (Bar Harbor, ME). Studies with ovariectomized (OVX) mice were compared to sham mice that had similar surgery without removal of the ovaries (Jackson Laboratories). Studies were conducted with C57BL/6J male mice injected subcutaneously with 250 ng of 17-β estradiol or an equal volume (50 μL) of vehicle (olive oil) daily for 21 days before silica exposure. Silica (Min-U-Sil 5) was provided by A. Ghio [U.S. Environmental Protection Agency (EPA), Durham, NC]. The following chemicals were obtained from identified suppliers: isoflurane (Webster Veterinary, Devens, MA), ketasthesia (Butler-Schein, Dublin, OH), xylazine hydrochloride (MP Biomedicals, Solon, OH), SPP1 enzyme-linked immunosorbent assay (ELISA) and antibody (R&D Systems, Minneapolis, MN), and Masson’s trichrome reagents and hematoxylin (Sigma Chemicals, St. Louis, MO). Immunohistochemistry was performed using secondary antibodies with VECTASTAIN® Elite ABC (Vector Labs, Burlingame, CA) and aminoethyl carbazole substrate (Life Technologies, Camarillo, CA). All other chemicals and reagents were purchased from Thermo Fisher Scientific (Pittsburgh, PA).
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