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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

Preparation of CXCR4-overexpressing rat cardiomyocyte. (A) Schematic diagram of the recombinant adenoviral vector. The rat CXCR4-encoding gene as well as a scrambled DNA sequence were amplified with PCR and incorporated into CMV downstream in the Adeasy-1/shuttle backbone vector. (B) Cardiomyocytes appeared infected by nearly 100% after 48-hr adenoviral gene transfer, as indicated by the appearance of GFP fluorescence. No morphological changes were detected in control- and CXCR4-adenovirus-infected cells. (C) Representative Western blots and quantitative data analysis illustrating the expression level of CXCR4 in rat cardiomyocytes after CXCR4-adenoviral gene transfer. (n represents six independent experiments; *P < 0.05).
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fig02: Preparation of CXCR4-overexpressing rat cardiomyocyte. (A) Schematic diagram of the recombinant adenoviral vector. The rat CXCR4-encoding gene as well as a scrambled DNA sequence were amplified with PCR and incorporated into CMV downstream in the Adeasy-1/shuttle backbone vector. (B) Cardiomyocytes appeared infected by nearly 100% after 48-hr adenoviral gene transfer, as indicated by the appearance of GFP fluorescence. No morphological changes were detected in control- and CXCR4-adenovirus-infected cells. (C) Representative Western blots and quantitative data analysis illustrating the expression level of CXCR4 in rat cardiomyocytes after CXCR4-adenoviral gene transfer. (n represents six independent experiments; *P < 0.05).

Mentions: To investigate the potential effects of CXCR4 in cardiomyocytes, we generated an adenovirus containing the rat CXCR4 encoding gene and an adenovirus containing the non-translated nucleotide sequence as control (Fig.2A). Both viruses also contained the GFP gene. Nearly 100% of ventricular cardiomyocytes appeared infected after 48 hrs, as indicated by green fluorescence (Fig.2B). Western blots confirmed that the expression level of CXCR4 was increased by 2.5-fold in CXCR4-adenoviral infecting group when compared to control group (Fig.2C), and CXCR4-overexpressing cardiomyocytes elicited the decreased contractile function (Fig. S1) and the compromised calcium handling (Fig. S2) upon the stimulation of SDF-1α.


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)

Preparation of CXCR4-overexpressing rat cardiomyocyte. (A) Schematic diagram of the recombinant adenoviral vector. The rat CXCR4-encoding gene as well as a scrambled DNA sequence were amplified with PCR and incorporated into CMV downstream in the Adeasy-1/shuttle backbone vector. (B) Cardiomyocytes appeared infected by nearly 100% after 48-hr adenoviral gene transfer, as indicated by the appearance of GFP fluorescence. No morphological changes were detected in control- and CXCR4-adenovirus-infected cells. (C) Representative Western blots and quantitative data analysis illustrating the expression level of CXCR4 in rat cardiomyocytes after CXCR4-adenoviral gene transfer. (n represents six independent experiments; *P < 0.05).
© Copyright Policy - open-access
Related In: Results  -  Collection

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

fig02: Preparation of CXCR4-overexpressing rat cardiomyocyte. (A) Schematic diagram of the recombinant adenoviral vector. The rat CXCR4-encoding gene as well as a scrambled DNA sequence were amplified with PCR and incorporated into CMV downstream in the Adeasy-1/shuttle backbone vector. (B) Cardiomyocytes appeared infected by nearly 100% after 48-hr adenoviral gene transfer, as indicated by the appearance of GFP fluorescence. No morphological changes were detected in control- and CXCR4-adenovirus-infected cells. (C) Representative Western blots and quantitative data analysis illustrating the expression level of CXCR4 in rat cardiomyocytes after CXCR4-adenoviral gene transfer. (n represents six independent experiments; *P < 0.05).
Mentions: To investigate the potential effects of CXCR4 in cardiomyocytes, we generated an adenovirus containing the rat CXCR4 encoding gene and an adenovirus containing the non-translated nucleotide sequence as control (Fig.2A). Both viruses also contained the GFP gene. Nearly 100% of ventricular cardiomyocytes appeared infected after 48 hrs, as indicated by green fluorescence (Fig.2B). Western blots confirmed that the expression level of CXCR4 was increased by 2.5-fold in CXCR4-adenoviral infecting group when compared to control group (Fig.2C), and CXCR4-overexpressing cardiomyocytes elicited the decreased contractile function (Fig. S1) and the compromised calcium handling (Fig. S2) upon the stimulation of SDF-1α.

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