ip 3 r2 knockout adult mice  (Jackson Laboratory)

Journal: Human Molecular Genetics

Article Title: Genetic ablation of IP 3 receptor 2 increases cytokines and decreases survival of SOD1 G93A mice

doi: 10.1093/hmg/ddw190

Figure Lengend Snippet: Relative IP 3 R2 gene expression is increased in models of neurodegeneration and inflammation. ( A ) Relative gene expression of IP 3 R2 assessed by qPCR on ventral spinal cords of non-transgenic (ntg; n = 6), SOD1 WT (wt; n = 6), pre-symptomatic SOD1 G93A (pre-s; n = 6), symptomatic SOD1 G93A (s; n = 5) and end stage SOD1 G93A (es; n = 5) mice (ANOVA, Bonferroni post-hoc). ( B ) Relative IP 3 R2 gene expression analysed in the lumbar spinal cord of severely affected EAE-mice ( n = 3) and control mice ( n = 6) by qPCR (unpaired t- test). ( C ) Relative IP 3 R2 gene expression analysed in the penumbra zone of stroke in mice ( n = 4) and a similar region in the contralateral side of the brain by qPCR (paired t -test). ( D ) Relative IP 3 R2 gene expression in ventral spinal cord astrocytes in vitro by 24 h LPS application ( n = 8) or vehicle ( n = 8; unpaired t -test). ( E ) Relative IP 3 R2 gene expression in murine macrophages ( n = 4; Wilcoxon signed rank test compared to 1.0, two-tailed). The dotted line reflects the normalising vehicle condition set at 1. Mean ± standard deviation. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001.

Article Snippet: IP 3 R2 knockout mice, described previously , were intercrossed with high-copy number SOD1 G93A (The Jackson Laboratory, Bar Harbor, USA).

Techniques: Gene Expression, Transgenic Assay, Control, In Vitro, Two Tailed Test, Standard Deviation

Journal: Human Molecular Genetics

Article Title: Genetic ablation of IP 3 receptor 2 increases cytokines and decreases survival of SOD1 G93A mice

doi: 10.1093/hmg/ddw190

Figure Lengend Snippet: IP 3 R2 knockout exacerbates disease in SOD1 G93A mice. Relative gene expression of IP 3 R1 ( A ), IP 3 R2 ( B ) and IP 3 R3 ( C ) assessed by qPCR in ventral spinal cords of IP 3 R2 +/+ ( n = 6), IP 3 R2 +/- ( n = 6) and IP 3 R2 -/- ( n = 6) mice. ( D ) Early symptom onset as determined by the hanging wire test between IP 3 R2 +/+ SOD1 G93A ( n = 6; 129.7 ± 8.6 days), IP 3 R2 +/- SOD1 G93A ( n = 7; 126.8 ± 9.1 days) and IP 3 R2 -/- SOD1 G93A mice ( n = 7; 126.4 ± 8.1 days, Log-rank, P = 0.88). ( E ) Late symptom onset as determined by the rotarod test between IP 3 R2 +/+ SOD1 G93A ( n = 6; 141.2 ± 5.1 days), IP 3 R2 +/- SOD1 G93A ( n = 7; 142.6 ± 5.4 days) and IP 3 R2 -/- SOD1 G93A mice ( n = 7; 138.7 ± 6.0 days, Log-rank, P = 0.55). ( F ) Survival analysis by determining the age of end stage of IP 3 R2 +/+ SOD1 G93A ( n = 19; 170.7 ± 9.6 days), IP 3 R2 +/- SOD1 G93A (n= 17; 162.8 ± 9.6 days) and IP 3 R2 -/- SOD1 G93A ( n = 18; 153.2 ± 12.5 days; Log-rank, P < 0.0001). ( G-H ) Disease progression as measured by grip strength of IP 3 R2 +/+ SOD1 G93A mice ( n = 5), IP 3 R2 +/- SOD1 G93A mice ( n = 7), IP 3 R2 -/- SOD1 G93A mice ( n = 6) and IP 3 R2 -/- mice ( n = 4) for the fore limbs (G) and all limbs (H). ( I ) Quantification of neurons from lumbar spinal cord in adult IP 3 R2 +/+ ( n = 3) , IP 3 R2 -/- ( n = 3) and 145 day old IP 3 R2 +/+ SOD1 G93A ( n = 3) and IP 3 R2 -/- SOD1 G93A mice ( n = 2; 2-way ANOVA disease stage P = 0.0061). ( J ) The viability of murine motor neurons isolated from IP 3 R2 -/- ( n = 4) and non-transgenic ( n = 4) plated on non-transgenic rat astrocytic feeder layers in serum-enriched media. Mean ± standard deviation.

Article Snippet: IP 3 R2 knockout mice, described previously , were intercrossed with high-copy number SOD1 G93A (The Jackson Laboratory, Bar Harbor, USA).

Techniques: Knock-Out, Gene Expression, Biomarker Discovery, Isolation, Transgenic Assay, Standard Deviation