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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

Cytosolic calcium overload in response to hypoxia/reoxygenation. (A) Representative flow cytometry histogram illustrating the distribution of asante calcium red (ACR) positive cardiomyocytes in the presence or absence of H/R. (B) Quantitative analysis of cytosolic Ca2+ concentration ([Ca2+]c) based on ACR fluorescence intensities, which are expressed as fold change relative to control group under normal condition. n represents six independent experiments; *P < 0.05 versus control group under normal condition; #P < 0.05 versus CXCR4 group under normal condition.
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fig03: Cytosolic calcium overload in response to hypoxia/reoxygenation. (A) Representative flow cytometry histogram illustrating the distribution of asante calcium red (ACR) positive cardiomyocytes in the presence or absence of H/R. (B) Quantitative analysis of cytosolic Ca2+ concentration ([Ca2+]c) based on ACR fluorescence intensities, which are expressed as fold change relative to control group under normal condition. n represents six independent experiments; *P < 0.05 versus control group under normal condition; #P < 0.05 versus CXCR4 group under normal condition.

Mentions: Calcium overload is a cellular consequence of I/R injury resulting from a disorder in cell membrane calcium ion transporting mechanisms. This calcium overload can subsequently damage functions of cellular organelles and initiate cell death. Under basal conditions, there was no difference in cytosolic calcium concentration between control and CXCR4 group (Fig.3A and B). Calcium concentration was increased 1.35-fold in the control group compared to normal conditions in response to H/R. Although calcium overload was also induced in CXCR4 group, there was no statistical difference between control and CXCR4 overexpressing group under H/R conditions.


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)

Cytosolic calcium overload in response to hypoxia/reoxygenation. (A) Representative flow cytometry histogram illustrating the distribution of asante calcium red (ACR) positive cardiomyocytes in the presence or absence of H/R. (B) Quantitative analysis of cytosolic Ca2+ concentration ([Ca2+]c) based on ACR fluorescence intensities, which are expressed as fold change relative to control group under normal condition. n represents six independent experiments; *P < 0.05 versus control group under normal condition; #P < 0.05 versus CXCR4 group under normal condition.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4549033&req=5

fig03: Cytosolic calcium overload in response to hypoxia/reoxygenation. (A) Representative flow cytometry histogram illustrating the distribution of asante calcium red (ACR) positive cardiomyocytes in the presence or absence of H/R. (B) Quantitative analysis of cytosolic Ca2+ concentration ([Ca2+]c) based on ACR fluorescence intensities, which are expressed as fold change relative to control group under normal condition. n represents six independent experiments; *P < 0.05 versus control group under normal condition; #P < 0.05 versus CXCR4 group under normal condition.
Mentions: Calcium overload is a cellular consequence of I/R injury resulting from a disorder in cell membrane calcium ion transporting mechanisms. This calcium overload can subsequently damage functions of cellular organelles and initiate cell death. Under basal conditions, there was no difference in cytosolic calcium concentration between control and CXCR4 group (Fig.3A and B). Calcium concentration was increased 1.35-fold in the control group compared to normal conditions in response to H/R. Although calcium overload was also induced in CXCR4 group, there was no statistical difference between control and CXCR4 overexpressing group under H/R conditions.

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