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1.
Fig. 5.

Fig. 5. From: Decreased tetrahydrobiopterin and disrupted association of Hsp90 with eNOS by hyperglycemia impair myocardial ischemic preconditioning.

GEL blocked infarct size reduction produced by IPC. A: ratio of Hsp90 to eNOS; B: myocardium at risk for infarction expressed as a percentage of left ventricle; C: infarct size expressed as a percentage of risk area. *P < 0.05 vs. CON; P < 0.05 vs. IPC (n = 6–7 mice/group).

Nikolina Vladic, et al. Am J Physiol Heart Circ Physiol. 2011 November;301(5):H2130-H2139.
2.
Fig. 3.

Fig. 3. From: Decreased tetrahydrobiopterin and disrupted association of Hsp90 with eNOS by hyperglycemia impair myocardial ischemic preconditioning.

Effects of DAHP on cardiac BH4 concentrations (A), area at risk for infarction (B), and myocardial infarct size (C) in rabbits subjected to ischemia and reperfusion injury in the absence (CON) or presence of IPC. *P < 0.05 vs. CON; ‡P < 0.05 vs. IPC (n = 8 rabbits/group).

Nikolina Vladic, et al. Am J Physiol Heart Circ Physiol. 2011 November;301(5):H2130-H2139.
3.
Fig. 2.

Fig. 2. From: Decreased tetrahydrobiopterin and disrupted association of Hsp90 with eNOS by hyperglycemia impair myocardial ischemic preconditioning.

Effects of intravenous d-glucose in the absence (CON) or presence of IPC with or without SEP on blood glucose concentration (A), BH4 (B), area of myocardium at risk for infarction (C), and infarct size (D) in rabbits subjected to ischemia (Isch) and reperfusion injury. *P < 0.05 vs. CON; †P < 0.05 vs. HG; ‡P < 0.05 vs. IPC; §P < 0.05 vs. HG + IPC (n = 6–8 rabbits/group).

Nikolina Vladic, et al. Am J Physiol Heart Circ Physiol. 2011 November;301(5):H2130-H2139.
4.
Fig. 8.

Fig. 8. From: Decreased tetrahydrobiopterin and disrupted association of Hsp90 with eNOS by hyperglycemia impair myocardial ischemic preconditioning.

HP and SEP increased eNOS dimerization in cultured endothelial cells. A: protein band density of eNOS monomer and dimer; B: representative Western blot bands of eNOS monomer and dimer from endothelial cells cultured in media containing 5.5 mM glucose. HP was induced by 3 cycles of 3 h of hypoxia/1 h of normoxia. The cells were treated for 1 h with 10 μM SEP before HP and between hypoxia. *P < 0.05 vs. CON; ‡P < 0.05 vs. HP (n = 3 cell dishes/group).

Nikolina Vladic, et al. Am J Physiol Heart Circ Physiol. 2011 November;301(5):H2130-H2139.
5.
Fig. 6.

Fig. 6. From: Decreased tetrahydrobiopterin and disrupted association of Hsp90 with eNOS by hyperglycemia impair myocardial ischemic preconditioning.

Calcium ionophore A-23187 (A23) increased the ratio of Hsp90-eNOS association in cultured endothelial cells (A) exposed to normal (CON) but not high glucose (HG) as determined by immunoprecipitation (IP, B) of eNOS and immunoblotting (IB) for eNOS and Hsp90. Lysate (L) represents total protein before IP, and supernatant (SN) represents protein after IP of eNOS. C: nitric oxide (NO) concentrations expressed as a percentage of CON. *P < 0.05 vs. CON; †P < 0.05 vs. A23 (n = 5–8/group).

Nikolina Vladic, et al. Am J Physiol Heart Circ Physiol. 2011 November;301(5):H2130-H2139.
6.
Fig. 7.

Fig. 7. From: Decreased tetrahydrobiopterin and disrupted association of Hsp90 with eNOS by hyperglycemia impair myocardial ischemic preconditioning.

HG blocked hypoxic preconditioning (HP)-elicited increases in the ratio of phosphorylated (Phos) eNOS/eNOS in endothelial cells. A: ratio of Phos-eNOS/eNOS; B: Western blot analysis of proteins from endothelial cells cultured in media containing 5.5 mM (CON and IPC) or 20 mM (HG and HP + HG) glucose. HP was induced by 3 consecutive hypoxia periods for 3 h, each followed by 1 h of normoxia. *P < 0.05 vs. CON; †P < 0.05 vs. HG; ‡P < 0.05 vs. HP (n = 4 cell dishes/group).

Nikolina Vladic, et al. Am J Physiol Heart Circ Physiol. 2011 November;301(5):H2130-H2139.
7.
Fig. 4.

Fig. 4. From: Decreased tetrahydrobiopterin and disrupted association of Hsp90 with eNOS by hyperglycemia impair myocardial ischemic preconditioning.

HG abolished increases in Hsp90-eNOS association and decreases in myocardial infarct size produced by IPC. A: blood glucose concentrations at baseline (time 0) and during ischemia and reperfusion; B: ratio of Hsp90/eNOS; C: myocardium at risk for infarction expressed as a percentage of left ventricle; D: infarct size expressed as a percentage of area at risk; E–H: representative photomicrographs of myocardial infarction in CON, HG, IPC, and IPC + HG mice, respectively. The hearts were stained with 2,3,5-triphenyltetrazolium chloride and phthalol blue dye to delineate the area at risk (red plus white areas) and infarct size (white areas). *P < 0.05 vs. CON; ‡P < 0.05 vs. IPC (n = 5–7 mice/group).

Nikolina Vladic, et al. Am J Physiol Heart Circ Physiol. 2011 November;301(5):H2130-H2139.
8.
Fig. 1.

Fig. 1. From: Decreased tetrahydrobiopterin and disrupted association of Hsp90 with eNOS by hyperglycemia impair myocardial ischemic preconditioning.

Schematic diagram depicting the experimental protocols. The effects of hyperglycemia (HG) with or without sepiapterin (SEP, protocol 1; A) or diamino-6-hydroxypyrimidine (DAHP, protocol 2; B) on myocardial tetrahydrobiopterin (BH4) and infarct size were determined in rabbits subjected to ischemia and reperfusion injury in the absence [control (CON)] or presence of ischemic preconditioning (IPC). The effects of HG (protocol 3; C) or geldanamycin (GEL, protocol 4; D) on heat shock protein 90 (Hsp90)-endothelial nitric oxide synthase (eNOS) association and infarct size in mice subjected to ischemia and reperfusion injury in the absence or presence of IPC. DMSO, dimethyl sulfoxide.

Nikolina Vladic, et al. Am J Physiol Heart Circ Physiol. 2011 November;301(5):H2130-H2139.

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