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Preservation of TSPO by chronic intermittent hypobaric hypoxia confers antiarrhythmic activity.

Li J, Xu J, Xiao J, Zhang H, Liang D, Liu Y, Zhang Y, Liu Y, Wen W, Hu Y, Yu Z, Yan B, Jiang B, Zhou ZN, Chen YH - J. Cell. Mol. Med. (2011)

Bottom Line: TSPO stimulation or inhibition affected the arrhythmias incidence in normoxic rats, but did not change the CIHH-mediated antiarrhythmic effects.The preservation of TSPO activity by CIHH also contributed to the maintenance of intracellular Ca homeostasis.These results suggest that the blunt sensitivity of TSPO to ischaemic stress may be responsible for the antiarrhythmic effects by CIHH.

View Article: PubMed Central - PubMed

Affiliation: Key Laboratory of Arrhythmias, Ministry of Education of China, Shanghai, China.

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Modulations of CIHH on translocator protein (TSPO). (A) Representative binding curves for TSPO in normoxic rat hearts that underwent stress-induced ventricular fibrillation (VF) protocol. (B) Stepwise elevation of Bmax was positively linked to ischaemic VF. CIHH up-regulated and preserved TSPO throughout normal and low-flow perfusion. (CIHH: chronic intermittent hypobaric hypoxia; *P, 0.05; **P, 0.01). (C) Regulation of Kd (equilibration dissociation constant) by ischaemia and CIHH (*P, 0.05). (D) Modification of TSPO mRNA expression by ischaemia and CIHH (*P, 0.05).
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fig02: Modulations of CIHH on translocator protein (TSPO). (A) Representative binding curves for TSPO in normoxic rat hearts that underwent stress-induced ventricular fibrillation (VF) protocol. (B) Stepwise elevation of Bmax was positively linked to ischaemic VF. CIHH up-regulated and preserved TSPO throughout normal and low-flow perfusion. (CIHH: chronic intermittent hypobaric hypoxia; *P, 0.05; **P, 0.01). (C) Regulation of Kd (equilibration dissociation constant) by ischaemia and CIHH (*P, 0.05). (D) Modification of TSPO mRNA expression by ischaemia and CIHH (*P, 0.05).

Mentions: As illustrated in Figure 2A and B, ischaemic VF was positively linked to TSPO activity alterations; specifically, ischaemic VF occurrence accompanied by stepped-up elevation of the protein activity. Of note, TSPO activity was higher in CIHH rats than in normoxic ones under basal conditions, and was preserved during ischaemia (Fig. 2B and C). Further analysis indicated that ischaemia did not modify the TSPO mRNA expression in normoxic rats. However, the level of TSPO expression was higher in CIHH rats than in normoxic ones under basal conditions, and was preserved throughout ischaemia (Fig. 2D). This evidence strongly supports the idea that CIHH blunts or resets the sensitivity of TSPO to ischaemic stress and further contributes to antiarrhythmia.


Preservation of TSPO by chronic intermittent hypobaric hypoxia confers antiarrhythmic activity.

Li J, Xu J, Xiao J, Zhang H, Liang D, Liu Y, Zhang Y, Liu Y, Wen W, Hu Y, Yu Z, Yan B, Jiang B, Zhou ZN, Chen YH - J. Cell. Mol. Med. (2011)

Modulations of CIHH on translocator protein (TSPO). (A) Representative binding curves for TSPO in normoxic rat hearts that underwent stress-induced ventricular fibrillation (VF) protocol. (B) Stepwise elevation of Bmax was positively linked to ischaemic VF. CIHH up-regulated and preserved TSPO throughout normal and low-flow perfusion. (CIHH: chronic intermittent hypobaric hypoxia; *P, 0.05; **P, 0.01). (C) Regulation of Kd (equilibration dissociation constant) by ischaemia and CIHH (*P, 0.05). (D) Modification of TSPO mRNA expression by ischaemia and CIHH (*P, 0.05).
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC3822500&req=5

fig02: Modulations of CIHH on translocator protein (TSPO). (A) Representative binding curves for TSPO in normoxic rat hearts that underwent stress-induced ventricular fibrillation (VF) protocol. (B) Stepwise elevation of Bmax was positively linked to ischaemic VF. CIHH up-regulated and preserved TSPO throughout normal and low-flow perfusion. (CIHH: chronic intermittent hypobaric hypoxia; *P, 0.05; **P, 0.01). (C) Regulation of Kd (equilibration dissociation constant) by ischaemia and CIHH (*P, 0.05). (D) Modification of TSPO mRNA expression by ischaemia and CIHH (*P, 0.05).
Mentions: As illustrated in Figure 2A and B, ischaemic VF was positively linked to TSPO activity alterations; specifically, ischaemic VF occurrence accompanied by stepped-up elevation of the protein activity. Of note, TSPO activity was higher in CIHH rats than in normoxic ones under basal conditions, and was preserved during ischaemia (Fig. 2B and C). Further analysis indicated that ischaemia did not modify the TSPO mRNA expression in normoxic rats. However, the level of TSPO expression was higher in CIHH rats than in normoxic ones under basal conditions, and was preserved throughout ischaemia (Fig. 2D). This evidence strongly supports the idea that CIHH blunts or resets the sensitivity of TSPO to ischaemic stress and further contributes to antiarrhythmia.

Bottom Line: TSPO stimulation or inhibition affected the arrhythmias incidence in normoxic rats, but did not change the CIHH-mediated antiarrhythmic effects.The preservation of TSPO activity by CIHH also contributed to the maintenance of intracellular Ca homeostasis.These results suggest that the blunt sensitivity of TSPO to ischaemic stress may be responsible for the antiarrhythmic effects by CIHH.

View Article: PubMed Central - PubMed

Affiliation: Key Laboratory of Arrhythmias, Ministry of Education of China, Shanghai, China.

Show MeSH
Related in: MedlinePlus