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Results: 6

1.
Figure 4

Figure 4. From: ?2-Adrenergic Receptors Mediate Cardioprotection through Crosstalk with Mitochondrial Cell Death Pathways.

Complex I and II activities are normal at baseline and decrease only in DOX treated β2-/- mice; *p<0.05 compared to WT.

Giovanni Fajardo, et al. J Mol Cell Cardiol. ;51(5):781-789.
2.
Figure 3

Figure 3. From: ?2-Adrenergic Receptors Mediate Cardioprotection through Crosstalk with Mitochondrial Cell Death Pathways.

β2-ARs attenuate mitochondrial dysfunction in DOX cardiotoxicity. Electron micrographs of WT and β2-/- mice treated with 15 mg/kg DOX for 24 h in the presence of a p38 inhibitor show cristae disruption only in the ß2-/-.

Giovanni Fajardo, et al. J Mol Cell Cardiol. ;51(5):781-789.
3.
Figure 6

Figure 6. From: ?2-Adrenergic Receptors Mediate Cardioprotection through Crosstalk with Mitochondrial Cell Death Pathways.

Cyclosporine (CsA, an inhibitor of the MPT and of calcineurin) partially rescues β2-/- mice receiving 10 mg/kg DOX; FK506 (a calcineurin inhibitor which does not block the MPT) has no effect. The combination of Akt activation with prazosin (Pra) and inhibition of the MPT with cyclosporine (CsA) provides a synergistic cardioprotective effect against DOX cardiotoxicity, nearly eliminating the toxicity (mortality reduced to 12.5%). DOX n=20, CsA n=16, FK506 n=16, CsA + Pra n=8.

Giovanni Fajardo, et al. J Mol Cell Cardiol. ;51(5):781-789.
4.
Figure 5

Figure 5. From: ?2-Adrenergic Receptors Mediate Cardioprotection through Crosstalk with Mitochondrial Cell Death Pathways.

β2-ARs regulate Ca2+ signaling and enhance opening of the MPT. A) Representative Ca2+ transients from WT and β2-/- mice. B) The rate of Ca2+ release is increased at baseline in β2-/- vs. WT mice; n=14, *p<0.05. C) Baseline peak [Ca2+]i is increased at baseline in β2-/- vs. WT mice; n=14, *p<0.05 compared to WT. D) Intrasarcomeric shortening was similar between WT and β2-/-; p=NS. E) The L-type calcium channel blocker verapamil reduces mortality in β2-/- mice receiving 10 mg/kg DOX; DOX n=20, verapamil n=8.

Giovanni Fajardo, et al. J Mol Cell Cardiol. ;51(5):781-789.
5.
Figure 1

Figure 1. From: ?2-Adrenergic Receptors Mediate Cardioprotection through Crosstalk with Mitochondrial Cell Death Pathways.

β2-ARs mediate cardioprotection through differential regulation of PKC isozymes. A) Baseline δPKC and εPKC levels in hearts from β2-/- and WT mice; Western blot image (top) and bar graph summarizing densitometry data (bottom); n=3, *p<0.05. B) δPKC is decreased and δPKC is increased in β2-/- vs. WT after 15 mg/kg DOX. Western blot image (top) and bar graph summarizing densitometry data (bottom); n=3, *p<0.01. C) The εPKC activator ψεRACK, but not the δPKC inhibitor δV1-1, reduces mortality in β2-/- mice receiving DOX at 8 mg/kg (LD50) dose; DOX alone n=16, δV1-1 n=10, ψεRACK n=15.

Giovanni Fajardo, et al. J Mol Cell Cardiol. ;51(5):781-789.
6.
Figure 2

Figure 2. From: ?2-Adrenergic Receptors Mediate Cardioprotection through Crosstalk with Mitochondrial Cell Death Pathways.

β2-ARs mediate cardioprotection through Akt signaling. A) Akt levels were similar in WT and β2-/- mice before and after DOX; Western blot image (top) and bar graph summarizing densitometry data (bottom); n=3, p=NS. B) Phosphorylation of Akt Ser 473 was lower in the β2-/- compared to WT at baseline. Only WT mice showed a decrease in phosphorylation of Akt after DOX, achieving levels similar to those in β2-/- DOX-treated mice; Western blot image (top) and bar graph summarizing densitometry data (bottom); n=3, *p<0.05 compared to WT, #p<0.05 compared to non-treated. C) Baseline and DOX-treated Akt activity is shown. Akt activation is markedly decreased only in DOX treated β2-/- mice. IP-kinase Akt activity assay (phospho-GSK3β); Western blot image (top) and bar graph summarizing densitometry data (bottom); n=4, *p<0.05. D) Prazosin restores Akt activity in DOX treated β2-/- mice; Western blot image (top) and bar graph summarizing densitometry data (bottom); n=3, *p<0.05. E) Prazosin reduces mortality in β2-/- mice receiving 10 mg/kg DOX; DOX n=20, prazosin n=11.

Giovanni Fajardo, et al. J Mol Cell Cardiol. ;51(5):781-789.

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