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Results: 7

1.
Fig. 2.

Fig. 2. From: Social stress in mice induces voiding dysfunction and bladder wall remodeling.

Bladder wall hypertrophy develops with exposure to the social stress as per the protocol outlined in Fig. 1. The y-axis represents the bladder mass (in mg) divided by the body mass (in g). Number of subjects is indicated in parentheses.

Andy Chang, et al. Am J Physiol Renal Physiol. 2009 October;297(4):F1101-F1108.
2.
Fig. 3.

Fig. 3. From: Social stress in mice induces voiding dysfunction and bladder wall remodeling.

Voiding phenotype is altered by social stress with an increase seen in the average voided volume and a decrease in the frequency. These values represent the average ± SD from 10 control and 10 stressed mice.

Andy Chang, et al. Am J Physiol Renal Physiol. 2009 October;297(4):F1101-F1108.
3.
Fig. 6.

Fig. 6. From: Social stress in mice induces voiding dysfunction and bladder wall remodeling.

Social stress leads to increased expression of the myosin heavy chain B and A mRNA isoforms. A representative gel with normalization to 18S RNA is shown. These values represent the average ± SD from 6 control (only 4 are shown) and 6 stressed mice.

Andy Chang, et al. Am J Physiol Renal Physiol. 2009 October;297(4):F1101-F1108.
4.
Fig. 1.

Fig. 1. From: Social stress in mice induces voiding dysfunction and bladder wall remodeling.

Schematic representation of the behavioral protocol used to induce social stress voiding dysfunction. The identification of aggressive C57 males from a population of retired breeders was made by observation when these mice were placed with a 6-wk-old FVB male. C57 mice were deemed aggressive if they attacked the FVB mouse in under 5 min. Approximately one-third of C57 mice screened met this criteria. Mice were separated as soon as any bite resulted in bleeding.

Andy Chang, et al. Am J Physiol Renal Physiol. 2009 October;297(4):F1101-F1108.
5.
Fig. 7.

Fig. 7. From: Social stress in mice induces voiding dysfunction and bladder wall remodeling.

Social stress leads to increased DNA synthesis in the bladder wall as measured by BrdU uptake. The values in the graph represent the means ± SD from 5 control and 5 stress mice. Images shown are color merged; therefore, nuclei staining pink are those with BrdU uptake as highlighted by the arrows. Blue nuclei are those in which no BrdU uptake is noted. S, serosal surface; M, mucosal surface.

Andy Chang, et al. Am J Physiol Renal Physiol. 2009 October;297(4):F1101-F1108.
6.
Fig. 4.

Fig. 4. From: Social stress in mice induces voiding dysfunction and bladder wall remodeling.

Representative in vivo cystometrograms from control (A) and stress (B) mice show a higher volume at micturition that was characteristic of the stress group. With social stress, the volume at micturition nearly doubled from 88 to 179 μl with P < 0.01 (C). There were no differences in micturition pressure or the threshold pressure at which voiding was initiated. It was noted that in the stress group, the voided volume exceeded the infused volume by 13% ; in contrast, in the control group the voided volume was 10% less than the infused volume (D). While this difference did not reach significance, it does suggest that the prolonged bladder retention induced by social stress may have resulted in postobstructive diuresis. These bar graphs represent means ± SD of cystometry recordings from 8 stressed and 7 control mice.

Andy Chang, et al. Am J Physiol Renal Physiol. 2009 October;297(4):F1101-F1108.
7.
Fig. 5.

Fig. 5. From: Social stress in mice induces voiding dysfunction and bladder wall remodeling.

Gel shift assays were performed for nuclear factor of activated T cells (NFAT) and myocyte enhancing factor 2 (MEF-2) and quantified using the Licor IR probe sets. With social stress, there was a rise in the nuclear translocation of both NFAT and MEF-2 over that seen in controls. In the absence of nuclear protein fractions, signal was lost (lane 1) compared with the gel shift seen from nuclear proteins from a social stress bladder (lane 2). Signal intensity for both NFAT and MEF-2 was lost with the application of “cold” oligonucleotide probe to the reaction (lane 3). The specificity of the oligonucleotide probe for the transcription factors was also studied using monocloncal antibodies. With the addition of anti-NFATc3 mab, there was a loss of signal as previously described (lane 4). A similar loss of signal was seen with antibodies against NFATc4 (data not shown). With addition of the monoclonal antibody against the MEF-2b, a pronounced supershift (SS) was observed (lane 4). These values represent the average ± SD from 5 control and 5 stressed mice.

Andy Chang, et al. Am J Physiol Renal Physiol. 2009 October;297(4):F1101-F1108.

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