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Gene expression in mouse whole proliferative phase wounds in response to alterations in β-Catenin levels [induced post-injury].

ABSTRACT: β-Catenin is a regulator of cutaneous wound repair. The expression of genes that are modulated in response to changes in β-Catenin levels (stabilization and downregulation) in cutaneous mouse wounds, post injury, during the proliferative phase of repair, was investigated. We are particularly interested in genes that are modulated (in opposite directions) in response to both the induction (stabilization) versus downregulation of β-Catenin. To investigate this, conditional β-Catenin stabilized (Harada, N., et al. EMBO J. 1999 Nov 1;18(21):5931-42) mice were injected with either a Cre-expressing adenovirus, or a GFP-expressing control virus, three days following injury, and wounds were harvested eight days post injury. For conditional knockdown of β-Catenin, mice generated from a cross between conditional β-Catenin knockdown mice (Brault, V. et al., Development. 2001 Apr;128(8):1253-64), and mice that express a tamoxifen-inducible form of Cre (Hayashi, S., and McMahon, A.P., Dev Biol. 2002 Apr 15;244(2):305-18), were treated with Tamoxifen for five days, beginning at the third day after injury. Wounds were harvested eight days after wounding. This provides insight into the identities of genes modulated in response to changes in β-Catenin levels during the proliferative stage of cutaneous wound repair.

ORGANISM(S): Mus musculus

PROVIDER: GSE50153 | GEO | 2018/12/31

REPOSITORIES: GEO

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Gene expression in mouse proliferative phase wounds in response to alterations in β-Catenin levels [initiated prior to injury].

Project description:β-Catenin is a regulator of cutaneous wound repair. The expression of genes that are modulated in response to changes in β-Catenin levels initiated prior to injury was investigated during the proliferative phase of repair. We are particularly interested in genes that are modulated (in opposite directions) in response to both the induction ('stabilization') versus downregulation of β-Catenin. To investigate this, conditional β-Catenin stabilized mice (Harada, N., et al. EMBO J. 1999 Nov 1;18(21):5931-42) were injected with either a Cre-expressing adenovirus, or a GFP-expressing control virus, four days prior to injury, and wounds were harvested eight days following injury. For conditional knockdown of β-Catenin, mice generated from a cross between conditional β-Catenin knockdown mice (Brault, V. et al., Development. 2001 Apr;128(8):1253-64), and mice that express a tamoxifen-inducible form of Cre (Hayashi, S., and McMahon, A.P., Dev Biol. 2002 Apr 15;244(2):305-18), were treated with Tamoxifen for five days prior to injury. Wounds were harvested eight days after wounding. This provides insight into gene expression changes that occur during the proliferative stage of cutaneous wound repair in response to changes in β-Catenin levels initiated before/at the time of injury.

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