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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

Mitochondrial STAT3 increased in CXCR4-overexpressing cardiomyocytes. (A) Representative Western blots illustrating the expression of STAT3, CoxIV, SERCA2a and GAPDH in mitochondrial- and cytosolic fraction. (B) Quantitative analysis of mitochondrial STAT3 expression level either in the absence or presence of H/R. n represents six independent experiments; *P < 0.05 versus control under normal condition, #P < 0.05 versus control under H/R condition.
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fig05: Mitochondrial STAT3 increased in CXCR4-overexpressing cardiomyocytes. (A) Representative Western blots illustrating the expression of STAT3, CoxIV, SERCA2a and GAPDH in mitochondrial- and cytosolic fraction. (B) Quantitative analysis of mitochondrial STAT3 expression level either in the absence or presence of H/R. n represents six independent experiments; *P < 0.05 versus control under normal condition, #P < 0.05 versus control under H/R condition.

Mentions: Cardiomyocyte mitochondria were isolated to examine further the possible mechanism underlying these CXCR4 OE-induced mitochondrial protective effects. The purification of isolated mitochondria was determined by the appearance of Cox IV using Western blot analysis, and this was confirmed without the detection of SERCA2a (SR marker) and GAPDH (cytosolic contaminant marker) in mitochondrial portion (Fig.5A). Both under basal and H/R conditions, the mitochondrial STAT3 expression level was enhanced to a greater extent in CXCR4 overexpressing cardiomyocytes than in the control group (Fig.5A and B).


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)

Mitochondrial STAT3 increased in CXCR4-overexpressing cardiomyocytes. (A) Representative Western blots illustrating the expression of STAT3, CoxIV, SERCA2a and GAPDH in mitochondrial- and cytosolic fraction. (B) Quantitative analysis of mitochondrial STAT3 expression level either in the absence or presence of H/R. n represents six independent experiments; *P < 0.05 versus control under normal condition, #P < 0.05 versus control under H/R condition.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

fig05: Mitochondrial STAT3 increased in CXCR4-overexpressing cardiomyocytes. (A) Representative Western blots illustrating the expression of STAT3, CoxIV, SERCA2a and GAPDH in mitochondrial- and cytosolic fraction. (B) Quantitative analysis of mitochondrial STAT3 expression level either in the absence or presence of H/R. n represents six independent experiments; *P < 0.05 versus control under normal condition, #P < 0.05 versus control under H/R condition.
Mentions: Cardiomyocyte mitochondria were isolated to examine further the possible mechanism underlying these CXCR4 OE-induced mitochondrial protective effects. The purification of isolated mitochondria was determined by the appearance of Cox IV using Western blot analysis, and this was confirmed without the detection of SERCA2a (SR marker) and GAPDH (cytosolic contaminant marker) in mitochondrial portion (Fig.5A). Both under basal and H/R conditions, the mitochondrial STAT3 expression level was enhanced to a greater extent in CXCR4 overexpressing cardiomyocytes than in the control group (Fig.5A and B).

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