p(MGI:Stat3, pmod(Ph))
Western-blot experiments revealed that LPS significantly stimulated of STAT3 phosphorylation in the spleen (Mann–Whitney U=0, Z=-2.309, P=0.021) (Fig. 8) and kidney (Mann–Whitney U=0, Z=-2.882, P=0.004) (data not shown) whereas anatabine significantly inhibited STAT3 phosphorylation in the spleen (Mann–Whitney U=1, Z=-2.021, P=0.043) and kidney (Mann– Whitney U=5, Z=-2.082, P=0.037) (data not shown) PubMed:23178521
A significant elevation of STAT3 phosphorylation was detected in the brain of Tg APPsw compared to their control littermates (Mann–Whitney U=1, Z=-3.767, p<0.001) and a significant reduction in STAT3 phosphorylation (Mann–Whitney U=8, Z=-2.066, p=0.039) was observed in the brain of Tg APPsw treated with anatabine compared to untreated Tg APPsw littermates (Fig. 10). PubMed:23178521
Western-blot experiments revealed that LPS significantly stimulated of STAT3 phosphorylation in the spleen (Mann–Whitney U=0, Z=-2.309, P=0.021) (Fig. 8) and kidney (Mann–Whitney U=0, Z=-2.882, P=0.004) (data not shown) whereas anatabine significantly inhibited STAT3 phosphorylation in the spleen (Mann–Whitney U=1, Z=-2.021, P=0.043) and kidney (Mann– Whitney U=5, Z=-2.082, P=0.037) (data not shown) PubMed:23178521
A significant elevation of STAT3 phosphorylation was detected in the brain of Tg APPsw compared to their control littermates (Mann–Whitney U=1, Z=-3.767, p<0.001) and a significant reduction in STAT3 phosphorylation (Mann–Whitney U=8, Z=-2.066, p=0.039) was observed in the brain of Tg APPsw treated with anatabine compared to untreated Tg APPsw littermates (Fig. 10). PubMed:23178521
We have shown previously that anatabine prevents STAT3 and p65 NFkB phosphorylation in various cell types and suggested that anatabine impact cytokine production by this mechanism as both STAT3 and p65 NFkB are known to regulate cytokine production. PubMed:23383175
Interestingly, a significant increase in STAT3 phosphorylation was observed in the spleen of EAE mice compared to control non immunized mice and a significant decrease in STAT3 phosphorylation level was detected in EAE mice treated with anatabine (Fig. 3) PubMed:23383175
Additionally, we observed that anatabine significantly prevented STAT3 and p65 NFkB phosphorylation in brain homogenates of EAE mice (Fig. 4) PubMed:23383175
A reduction in the number of phosphorylated STAT3 immunoreactive cells was observed in the cerebral cortex of EAE mice treated with anatabine further confirming the data obtained by western-blotting using brain homogenates (Fig. 5) PubMed:23383175
Similarly, we observed an increased number of phosphorylated STAT3 immunopositive cells in the spinal cord of EAE mice compared to control non-immunized mice and a decreased number of phosphorylated STAT3 immunoreactive cells in EAE mice treated with anatabine (Fig. 6) showing overall that anatabine reduces STAT3 phosphorylation in the brain, spinal cord and spleen of EAE mice. PubMed:23383175
In addition, we observed a statistically significant correlation between the amount of p65 NFkB phosphorylation and STAT3 phosphorylation in brain homogenates (Pearson Correlation = 0.637, P<0.001) PubMed:23383175
Interestingly, a statistically significant correlation was observed between the amount of STAT3 phosphorylation detected in brain homogenates and the clinical severity of EAE (Pearson correlation = 0.653, P<0.001) but not with p65 NFkB phosphorylation (Pearson correlation = 0.371, P= 0.062) suggesting that STAT3 may play a more preponderant role than NFkB in the development of neurological deficits of EAE PubMed:23383175
Interestingly, a significant increase in STAT3 phosphorylation was observed in the spleen of EAE mice compared to control non immunized mice and a significant decrease in STAT3 phosphorylation level was detected in EAE mice treated with anatabine (Fig. 3) PubMed:23383175
Western-blot experiments using brain homogenates from EAE mice also reveal that both STAT3 and p65 NFkB phosphorylation are significantly elevated in the brain of EAE mice compared to control non immunized mice (Fig. 4) PubMed:23383175
Interestingly, a statistically significant correlation was observed between the amount of STAT3 phosphorylation detected in brain homogenates and the clinical severity of EAE (Pearson correlation = 0.653, P<0.001) but not with p65 NFkB phosphorylation (Pearson correlation = 0.371, P= 0.062) suggesting that STAT3 may play a more preponderant role than NFkB in the development of neurological deficits of EAE PubMed:23383175
We further assessed STAT3 phosphorylation by immunohistochemistry using brain sections of the animals and observed an increased number of phosphorylated STAT3 immunopositive cells in the cortex of EAE mice compared to control non-immunized mice (Fig. 5) PubMed:23383175
Similarly, we observed an increased number of phosphorylated STAT3 immunopositive cells in the spinal cord of EAE mice compared to control non-immunized mice and a decreased number of phosphorylated STAT3 immunoreactive cells in EAE mice treated with anatabine (Fig. 6) showing overall that anatabine reduces STAT3 phosphorylation in the brain, spinal cord and spleen of EAE mice. PubMed:23383175
A statistically significant correlation was observed between the number of STAT3 phosphorylated cells in the cerebral cortex and the clinical severity of EAE (Pearson Correlation =0.531, P,0.002) PubMed:23383175
A statistically significant correlation was also observed between the amount of STAT3 phosphorylated cells in the spinal cord and the clinical severity of EAE (Pearson Correlation = 0.512, P,0.004) PubMed:23383175
Interestingly, a statistically significant correlation was observed between the amount of STAT3 phosphorylation detected in brain homogenates and the clinical severity of EAE (Pearson correlation = 0.653, P<0.001) but not with p65 NFkB phosphorylation (Pearson correlation = 0.371, P= 0.062) suggesting that STAT3 may play a more preponderant role than NFkB in the development of neurological deficits of EAE PubMed:23383175
A statistically significant correlation was observed between the number of STAT3 phosphorylated cells in the cerebral cortex and the clinical severity of EAE (Pearson Correlation =0.531, P,0.002) PubMed:23383175
A statistically significant correlation was also observed between the amount of STAT3 phosphorylated cells in the spinal cord and the clinical severity of EAE (Pearson Correlation = 0.512, P,0.004) PubMed:23383175
Interestingly, a statistically significant correlation was observed between the amount of STAT3 phosphorylation detected in brain homogenates and the clinical severity of EAE (Pearson correlation = 0.653, P<0.001) but not with p65 NFkB phosphorylation (Pearson correlation = 0.371, P= 0.062) suggesting that STAT3 may play a more preponderant role than NFkB in the development of neurological deficits of EAE PubMed:23383175
In addition, we observed a statistically significant correlation between the amount of p65 NFkB phosphorylation and STAT3 phosphorylation in brain homogenates (Pearson Correlation = 0.637, P<0.001) PubMed:23383175
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If you find BEL Commons useful in your work, please consider citing: Hoyt, C. T., Domingo-Fernández, D., & Hofmann-Apitius, M. (2018). BEL Commons: an environment for exploration and analysis of networks encoded in Biological Expression Language. Database, 2018(3), 1–11.