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Results: 6

1.
Figure 5

Figure 5. From: The HDAC inhibitors trichostatin A and suberoylanilide hydroxamic acid exhibit multiple modalities of benefit for the vascular pathobiology of sickle transgenic mice.

Iron chelation. Ferric ammonium citrate in buffer plus DMSO exhibits an absence of absorbance in the visible region (curve 1). Solutions of 3 chelators in DMSO were identical to curve 1. In contrast, iron chelation by 3 hydroxamic acids is illustrated by color development: curve 2, SAHA; curve 3, TSA; and curve 4, desferrioxamine. These data confirm iron chelation by all 3 hydroxamic acids, DFO, TSA, and SAHA.

Robert P. Hebbel, et al. Blood. 2010 March 25;115(12):2483-2490.
2.
Figure 1

Figure 1. From: The HDAC inhibitors trichostatin A and suberoylanilide hydroxamic acid exhibit multiple modalities of benefit for the vascular pathobiology of sickle transgenic mice.

qPCR quantitation of (whole-lung) pulmonary endothelial antigens. qPCr quantitation in NY1DD mice shows that the stress of H/R, compared with controls at ambient air, does increase level of murine TF mRNA (left panel; P = .023), and does not significantly increase the level of murine VCAM1 mRNA (middle panel; P = .119). In the right panel, level of a control mRNA (murine PECAM) does not change, as expected (P = .383). These measurements are consistent with the protein data shown in Figure 2. To obtain each data point (n = 4 for each antigen), endothelial cells from 3 mice had to be pooled for analysis. Error bars show ±SD.

Robert P. Hebbel, et al. Blood. 2010 March 25;115(12):2483-2490.
3.
Figure 4

Figure 4. From: The HDAC inhibitors trichostatin A and suberoylanilide hydroxamic acid exhibit multiple modalities of benefit for the vascular pathobiology of sickle transgenic mice.

Vascular stasis as monitored in a DSFC model using hBERK1 mice subjected to H/R. Mice were treated with or without TSA for 3 days. After the third TSA dose, flowing venules were selected and studied. Animals were then subjected to H/R. After 1 hour and 4 hours of reoxygenation, the same venules were re-examined for blood flow. There were 5 mice and 251 venules in the TSA-treated group, and 4 mice and 85 venules in the vehicle group. At least 18 venules per mouse were evaluable. Expressed on a per-total venule basis, asterisk (*) shows P = .006 for both at 1 hour and 4 hours of reoxygenation. This demonstrates an antistasis effect of TSA, consistent with that of other hydroxamic acids we previously studied using a different intravital microscopy model.15 Error bars show SE.

Robert P. Hebbel, et al. Blood. 2010 March 25;115(12):2483-2490.
4.
Figure 3

Figure 3. From: The HDAC inhibitors trichostatin A and suberoylanilide hydroxamic acid exhibit multiple modalities of benefit for the vascular pathobiology of sickle transgenic mice.

Dose response to TSA in the NY1DD mouse. VCAM (A) and TF (B) in the NY1DD mouse illustrate dose-response to TSA pretreatment. In both panels, the 2 leftmost open bars illustrate the already described (in Figure 1) status in NY1DD animals at air and after H/R. Black bars show effect of TSA pretreatment of NY1DD animals then exposed to H/R. (A) *P < .001; **P = .04; ***P = .002. (B) #P = .009; *P < .001; **P = .003. Number of animals for bars left to right: top panel, 4, 4, 6, 3, 3, and 3; bottom panel, 4, 4, 6, 3, 3, and 3.These data illustrate that a pretreatment TSA dose of 1 mg/kg is the minimal efficacious dose. Error bars show ±SD.

Robert P. Hebbel, et al. Blood. 2010 March 25;115(12):2483-2490.
5.
Figure 6

Figure 6. From: The HDAC inhibitors trichostatin A and suberoylanilide hydroxamic acid exhibit multiple modalities of benefit for the vascular pathobiology of sickle transgenic mice.

Effect of SAHA on sickle transgenic mice in vivo. Three-day pretreatment with SAHA diminished both VCAM (A) and TF (B) in the NY1DD mouse at air and after H/R. (A) *P < .001; **P < .001. (B) *P = .017. For panels A and B, the number of animals for bars left to right was 4, 5, 4, and 5, respectively. (C) In post-H/R S+SAntilles sickle animals, SAHA inhibits stasis measured at 1 hour and 4 hours of reoxygenation. with P = .006 for both (#). Number of observations was 4 animals and 236 venules in the vehicle-treated group, and 4 animals and 245 venules in the SAHA-treated group. Overall, these data demonstrate that the clinically approved analog, SAHA, exhibits the same spectrum of effects as TSA. Error bars show SD (A-B) or SE (C).

Robert P. Hebbel, et al. Blood. 2010 March 25;115(12):2483-2490.
6.
Figure 2

Figure 2. From: The HDAC inhibitors trichostatin A and suberoylanilide hydroxamic acid exhibit multiple modalities of benefit for the vascular pathobiology of sickle transgenic mice.

VCAM and TF in the control and sickle mouse. VCAM (A) and TF (B) in the C57BL6 control and NY1DD sickle mice, which were pretreated with TSA for 3 days; hBERK1 mice were treated for 3, 7, or 21 days only at ambient air. NY1DD mice were studied at air and after H/R, as indicated, whereas hBERK1 animals were studied only at air. (A) *P < .001; **P < .001; #P = .027; &P = .019. (B) *P < .001; #P = .029; and &P < .001. Number of experimental animals, for bars left to right: top panel, 8, 4, 8, 4, 4, 6, 4, 6, 6, 6, 6, and 6; bottom panel, 4, 4, 4, 4, 4, 6, 4, 6, 6, 6, 6, and 6. These data illustrate that TSA decreases expression of VCAM and TF when given as pretreatment before the H/R-induced boost in endothelial stimulation (NY1DD model). In the hBERK1 model, with already-boosted VCAM and TF at ambient air, the TSA reduced VCAM but not TF unless it was given for a prolonged period. Error bars show ±SD.

Robert P. Hebbel, et al. Blood. 2010 March 25;115(12):2483-2490.

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