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CXCR4 attenuates cardiomyocytes mitochondrial dysfunction to resist ischaemia-reperfusion injury.

Cai WF, Kang K, Huang W, Liang JL, Feng YL, Liu GS, Chang DH, Wen ZL, Paul C, Xu M, Millard RW, Wang Y - J. Cell. Mol. Med. (2015)

Bottom Line: The increased CXCR4 expression was observed in cardiomyocytes post CXCR4-adenovirus transduction and this OE significantly reduced the cardiomyocyte contractility under basal conditions.Interestingly, this CXCR4-induced mitochondrial protective effect is associated with the enhanced signal transducer and activator of transcription 3 (expression in mitochondria.Consequently, in the presence of H/R, mitochondrial dysfunction was mitigated and cardiomyocyte death was decreased to 65% in the CXCR4 OE group as compared with the control group.

View Article: PubMed Central - PubMed

Affiliation: Department of Pathology & Lab Medicine, College of Medicine, University of Cincinnati, Cincinnati, OH, USA.

No MeSH data available.


Related in: MedlinePlus

CXCR4 overexpression attenuated mitochondrial dysfunction in response to stress stimuli. (A) Representative histogram illustrating the distribution of TMRE-loaded cardiomyocytes according to the fluorescence intensity. (B) Quantitative analysis of the mean of TMRE intensity to illustrate mitochondrial membrane potential, which are expressed as fold change relative to control group under normal condition. (C) Absorbance at 520 nm was recorded to illustrate mitochondrial swelling either in the presence or absence of Ca2+ (250 nmol/l). (D) Absorbance at 520 nm was monitored to illustrate mitochondria swelling after Ca2+ stimulation in the presence of cyclosporine A (CSA; 1 μM) n represents six independent experiments; *P < 0.05 versus control group under normal condition; #P < 0.05 versus control group at the same time-point; §P < 0.05.
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fig04: CXCR4 overexpression attenuated mitochondrial dysfunction in response to stress stimuli. (A) Representative histogram illustrating the distribution of TMRE-loaded cardiomyocytes according to the fluorescence intensity. (B) Quantitative analysis of the mean of TMRE intensity to illustrate mitochondrial membrane potential, which are expressed as fold change relative to control group under normal condition. (C) Absorbance at 520 nm was recorded to illustrate mitochondrial swelling either in the presence or absence of Ca2+ (250 nmol/l). (D) Absorbance at 520 nm was monitored to illustrate mitochondria swelling after Ca2+ stimulation in the presence of cyclosporine A (CSA; 1 μM) n represents six independent experiments; *P < 0.05 versus control group under normal condition; #P < 0.05 versus control group at the same time-point; §P < 0.05.

Mentions: Elevated cytosolic calcium and oxidative stress will induce excessive mitochondrial Ca2+ entry, which can initiate mitochondrial permeability transition pore (mPTP) associating with dissipating the mitochondrial inner membrane potential (Δψm). Under basal conditions, Δψm was similar in control and CXCR4 overexpressing cardiomyocytes, as seen by the strong TMRE fluorescent intensity distribution (Fig.4A). In the presence of oxidative stress induced by hydrogen peroxide, the TMRE fluorescence intensity dissipated in a time-dependent manner (Fig.4A). Quantitative analysis of the flow cytometer data indicated that Δψm decreased by 30%, 50% and 64% at 1, 10 and 20 min. after hydrogen peroxide treatment, when compared to the basal condition. The reduction percentage of Δψm at the same points in CXCR4-transduced cardiomyocytes was 15%, 31% and 55% (Fig.4B).


CXCR4 attenuates cardiomyocytes mitochondrial dysfunction to resist ischaemia-reperfusion injury.

Cai WF, Kang K, Huang W, Liang JL, Feng YL, Liu GS, Chang DH, Wen ZL, Paul C, Xu M, Millard RW, Wang Y - J. Cell. Mol. Med. (2015)

CXCR4 overexpression attenuated mitochondrial dysfunction in response to stress stimuli. (A) Representative histogram illustrating the distribution of TMRE-loaded cardiomyocytes according to the fluorescence intensity. (B) Quantitative analysis of the mean of TMRE intensity to illustrate mitochondrial membrane potential, which are expressed as fold change relative to control group under normal condition. (C) Absorbance at 520 nm was recorded to illustrate mitochondrial swelling either in the presence or absence of Ca2+ (250 nmol/l). (D) Absorbance at 520 nm was monitored to illustrate mitochondria swelling after Ca2+ stimulation in the presence of cyclosporine A (CSA; 1 μM) n represents six independent experiments; *P < 0.05 versus control group under normal condition; #P < 0.05 versus control group at the same time-point; §P < 0.05.
© Copyright Policy - open-access
Related In: Results  -  Collection

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getmorefigures.php?uid=PMC4549033&req=5

fig04: CXCR4 overexpression attenuated mitochondrial dysfunction in response to stress stimuli. (A) Representative histogram illustrating the distribution of TMRE-loaded cardiomyocytes according to the fluorescence intensity. (B) Quantitative analysis of the mean of TMRE intensity to illustrate mitochondrial membrane potential, which are expressed as fold change relative to control group under normal condition. (C) Absorbance at 520 nm was recorded to illustrate mitochondrial swelling either in the presence or absence of Ca2+ (250 nmol/l). (D) Absorbance at 520 nm was monitored to illustrate mitochondria swelling after Ca2+ stimulation in the presence of cyclosporine A (CSA; 1 μM) n represents six independent experiments; *P < 0.05 versus control group under normal condition; #P < 0.05 versus control group at the same time-point; §P < 0.05.
Mentions: Elevated cytosolic calcium and oxidative stress will induce excessive mitochondrial Ca2+ entry, which can initiate mitochondrial permeability transition pore (mPTP) associating with dissipating the mitochondrial inner membrane potential (Δψm). Under basal conditions, Δψm was similar in control and CXCR4 overexpressing cardiomyocytes, as seen by the strong TMRE fluorescent intensity distribution (Fig.4A). In the presence of oxidative stress induced by hydrogen peroxide, the TMRE fluorescence intensity dissipated in a time-dependent manner (Fig.4A). Quantitative analysis of the flow cytometer data indicated that Δψm decreased by 30%, 50% and 64% at 1, 10 and 20 min. after hydrogen peroxide treatment, when compared to the basal condition. The reduction percentage of Δψm at the same points in CXCR4-transduced cardiomyocytes was 15%, 31% and 55% (Fig.4B).

Bottom Line: The increased CXCR4 expression was observed in cardiomyocytes post CXCR4-adenovirus transduction and this OE significantly reduced the cardiomyocyte contractility under basal conditions.Interestingly, this CXCR4-induced mitochondrial protective effect is associated with the enhanced signal transducer and activator of transcription 3 (expression in mitochondria.Consequently, in the presence of H/R, mitochondrial dysfunction was mitigated and cardiomyocyte death was decreased to 65% in the CXCR4 OE group as compared with the control group.

View Article: PubMed Central - PubMed

Affiliation: Department of Pathology & Lab Medicine, College of Medicine, University of Cincinnati, Cincinnati, OH, USA.

No MeSH data available.


Related in: MedlinePlus