B6.129 fvb col1a2tm1mcbr j

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B6.129(FVB)-Col1a2tm1Mcbr/J; is a transgenic mouse strain that carries a targeted mutation in the Col1a2 gene. The Col1a2 gene encodes the pro-α2 chain of type I collagen, which is a major structural component of the extracellular matrix. This strain can be used in research related to the study of collagen and its role in various biological processes.

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Lab products found in correlation

αmem glutamax, by Thermo Fisher Scientific (1 mentions) Ascorbic acid 2 phospate, by Merck Group (1 mentions) Fetal bovine serum (fbs), by Merck Group (1 mentions) Pen strep, by Corning (1 mentions) Blyscan, by Biocolor (1 mentions) Sircol, by Biocolor (1 mentions)

3 protocols using b6.129 fvb col1a2tm1mcbr j

Osteoblast Culturing and Extraction

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MC3T3-E1 Subclone 4 osteoblast cell lines were acquired from ATCC (ATCC CRL-2593). Cells were cultured in αMEM + Glutamax (32571-036; Gibco) supplemented with 10% FBS (Sigma-Aldrich) and 1% Pen/Strep (Corning). To stimulate procollagen synthesis and secretion, ascorbic acid 2-phospate (Sigma-Aldrich) was supplemented 18–24 h before imaging experiments.
Primary osteoblasts were extracted from mice harboring the G610C mutation and their wild-type littermates (B6.129(FVB)-Col1a2tm1Mcbr/J; Jackson Laboratories), which were maintained on the C57BL/6J background (4 (link), 23 (link)). Osteoblasts were extracted from parietal bones of 3- to 8-d-old mice as previously described (4 (link)). All care and procedures were performed in accordance with a Eunice Kennedy Shriver National Institute of Child Health and Human Development Animal Care and Use Committee-approved protocol.

Omari S., Makareeva E., Roberts-Pilgrim A., Mirigian L., Jarnik M., Ott C., Lippincott-Schwartz J, & Leikin S. (2018). Noncanonical autophagy at ER exit sites regulates procollagen turnover. Proceedings of the National Academy of Sciences of the United States of America, 115(43), E10099-E10108.

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Carbamazepine Treatment in Osteogenesis Imperfecta Mice

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Heterozygous α2(I)‐G610C mice (Col1a2^+/p.G610C)⁵ were obtained from Jackson Laboratory, Bar Harbour, ME, USA (B6.129[FVB]‐Col1a2^tm1Mcbr/J; stock 007248) and maintained on a C57BL/6J background to generate heterozygous Col1a2^+/p.G610C and control experimental mice. Mice husbandry and health monitoring are previously described.⁹ All procedures were approved by the Murdoch Children's Research Institute Animal Ethics Committee (#A798). Male control and Col1a2^+/p.G610C mice were treated by oral gavage with CBZ (250 mg/kg/day) from 3 to 6 weeks.¹¹, ¹² A second cohort was additionally treated from 6 to 9 weeks by subcutaneous implantation of a slow‐release pellet of carbamazepine (250 mg/kg/day) (Innovative Research of America USA C‐113).¹¹ At 6 and 9 weeks, mice were euthanased and tissues harvested.

Blank M., McGregor N.E., Rowley L., Kung L.H., Crimeen‐Irwin B., Poulton I.J., Walker E.C., Gooi J.H., Lamandé S.R., Sims N.A, & Bateman J.F. (2022). The effect of carbamazepine on bone structure and strength in control and osteogenesis imperfecta (Col1a2 +/p.G610C ) mice. Journal of Cellular and Molecular Medicine, 26(14), 4021-4031.

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Skeletal Characterization of Het G610C Mice

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Het G610C mice (B6.129(FVB)-Col1a2^tm1Mcbr/J) were purchased from Jackson Laboratories (stock # 007248) and maintained on the C57BL/6J background. Animal care and experiments were performed in accordance with a protocol approved by the NICHD ACUC. Skeletal staining was performed as described in the 2010 Woods Hole Mouse Embryology Module manual. RNA was extracted from freshly dissected parietal bones in Trizol. For Western Blots (WB), parietal bones were stored frozen until needed. For electron microscopy, parietal bones were fixed with 2.5 % glutaraldehyde or with 2% formaldehyde/2 % glutaraldehyde for 4 h at room temperature and then overnight at 4 °C. Collagen and glycosaminoglycan content in embryonic skin was measured with Sircol and Blyscan assays (Biocolor, UK), respectively.

Mirigian L.S., Makareeva E., Mertz E.L., Omari S., Roberts-Pilgrim A.M., Oestreich A.K., Phillips C.L, & Leikin S. (2016). Osteoblast malfunction caused by cell stress response to procollagen misfolding in α2(I)-G610C mouse model of osteogenesis imperfecta. Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research, 31(8), 1608-1616.

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